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Copyright ©The Author(s) 2025. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Stem Cells. Jul 26, 2025; 17(7): 105371
Published online Jul 26, 2025. doi: 10.4252/wjsc.v17.i7.105371
Combining acupuncture and mesenchymal stem cell therapy offers promise as a treatment for inflammatory bowel disease
Wei-Gang Ma, Yu-Xin Si, Yong-Long Zhang, Wei-Fang Gao, Yu-Ge Dong, Zhi-Fang Xu, Research Center of Experimental Acupuncture Science, Tianjin University of Traditional Chinese Medicine, Tianjin 301617, China
Yan-Qi Li, Qiang Xi, Department of Clinical Practice, Tianjin University of Traditional Chinese Medicine, Tianjin 301617, China
Zhong-Zheng Li, Research Center of Experimental Acupuncture Science, Tianjin University of Traditional Chinese Medicine, School of Acupuncture and Tuina, Tianjin 301617, China
ORCID number: Zhong-Zheng Li (0000-0002-3380-2793).
Co-first authors: Wei-Gang Ma and Yu-Xin Si.
Author contributions: Ma WG and Si YX contributed to the conceptualization; Ma WG wrote original draft; Zhang YL, Gao WF, and Dong YG participated in the investigation of this manuscript; Li YQ and Xi Q contributed to visualization; Xu ZF and Li ZZ participated in the review & editing of this article. Ma WG and Si YX contributed equally to this work as co-first authors of this manuscript.
Supported by the National Natural Science Foundation of China, No. 82174524.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Open Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Zhong-Zheng Li, Associate Professor, Research Center of Experimental Acupuncture Science, Tianjin University of Traditional Chinese Medicine, School of Acupuncture and Tuina, No. 10 Poyanghu Road, West Area, Tuanbo New Town, Jinghai District, Tianjin 301617, China. lizhzh2008@163.com
Received: January 20, 2025
Revised: March 25, 2025
Accepted: June 20, 2025
Published online: July 26, 2025
Processing time: 185 Days and 18.4 Hours

Abstract

Inflammatory bowel disease (IBD) is a persistent gastrointestinal ailment driven by a range of immunological and pathophysiological factors, and often exposes patients to persistent pain and a greater risk of tumor development. In clinical settings, sulfasalazine is among the most common treatments used to manage IBD, but such treatment can result in a range of side effects in addition to leading to relatively poor efficacy. In certain refractory cases, patients must undergo surgical resection of affected tissues, underscoring the need to devise safer and more efficacious forms of alternative treatment. Mesenchymal stem cells (MSCs) have recently been shown to exhibit been shown to exhibit robust immunomodulatory activity and potential for differentiation such that they may be an effective tool for treating IBD. Acupuncture has also shown promise as an efficacious treatment option for IBD, performing better than drug-based treatments in certain clinical trials. Acupuncture is capable of enhancing endogenous MSC proliferation and homing, enabling these cells to more effectively migrate toward target lesion sites and to promote tissue repair. In light of these findings, this review was formulated to survey the potential therapeutic advantages of combining MSCs and acupuncture when attempting to treat IBD.

Key Words: Acupuncture; Mesenchymal stem cell; Inflammatory bowel disease; Anti-inflammatory; Oxidative stress

Core Tip: This paper analyzes and summarizes previous studies and suggests that acupuncture combined with stem cell transplantation may be more effective than monotherapy in the treatment of inflammatory bowel disease and ensure safety. A systematic description of the possible mechanisms of action is provided to support the feasibility of this method.



INTRODUCTION

Inflammatory bowel disease (IBD) is an inflammatory form of gastrointestinal disease that can be further categorized into Crohn’s disease (CD) and ulcerative colitis (UC) based on the histological findings in affected patients[1]. IBD pathogenesis is associated with a variety of environmental, genetic, and immune-related factors[2]. A population-based study in Quebec, Canada[3] showed that patients with CD and UC had significantly higher all-cause mortality rates than the general population, with standardized mortality ratios of 1.45 and 2.21 for patients with CD and UC, respectively, while the 10-year trial showed increases in all-cause mortality of approximately 40% in patients with CD and 20% in those with UC, with about 33% of patients dying of cancer. The same trend was observed in another study[4] where the risk of death and cancer was found to be significantly higher in patients with IBD than in the general population. IBD is increasingly common among older adults, even though it was historically thought to primarily impact younger individuals[5,6]. Global IBD incidence rates are also rising[7], underscoring the need for additional efforts to mitigate this rise and associated risk. One key facet of this interventional approach is the diversification of therapeutic modalities. At present IBD treatments in the clinic primarily entail the use of sulfasalazine and other aminosalicylate compounds, leading to inevitable side effects, such as high blood pressure, fatigue, and increased risk of infection, while the use of immunosuppressive drugs can be life-threatening[8]. Stem cell transplantation has recently exhibited great potential as a therapeutic strategy, with preclinical evidence supporting the use of mesenchymal stem cells (MSCs) extracted from embryonic tissue as tools that can help alleviate IBD[9], while clinical trials have further highlighted the therapeutic benefits of these MSCs in IBD[10]. While MSC therapy is impacted by factors including MSC type, timing, transplantation approach, and homing effects[11,12], it nonetheless provides some attractive advantages relative to pharmacological treatment, including genetic stability, greater accessibility, low levels of immunogenicity, and strong immunomodulatory activity[13].

Acupuncture offers significant utility as an approach to treating a growing number of diseases and disorders. Contemporary clinical acupuncture modalities primarily comprise manual acupuncture (MA) and electroacupuncture (EA), each with distinct operational frameworks and therapeutic advantages. MA involves the selection of disease-specific acupoints, followed by rapid needle insertion using techniques such as tube-assisted or rotational insertion to minimize discomfort. Skilled acupuncturists then manipulate needles through lifting-thrusting or twirling methods to elicit the Deqi sensation - characterized by localized soreness, numbness, or distension - adjusted to patient tolerance. This modality relies on periodic interventions to restore physiological balance, making it particularly suitable for chronic conditions requiring individualized modulation of immune and visceral functions. In contrast, EA enhances traditional needle stimulation through programmable electrical pulses, enabling precise neuromodulation. After achieving target needle depth, electrodes are attached to deliver frequency-specific stimulation, with intensity calibrated to induce subtle muscle contractions without pain. EA’s standardized parameters and quantifiable output not only improve reproducibility in research settings but also amplify therapeutic efficacy in scenarios demanding targeted anti-inflammatory or neuroregulatory effects, such as chronic pain management and synergistic applications with stem cell therapies. Consequently, while MA excels in holistic functional regulation, EA’s technological precision establishes it as the preferred modality for mechanistically driven translational studies.

In several preclinical and clinical analyses, acupuncture has been found to exert analgesic, anti-inflammatory, and immunomodulatory effects[14-18], with a steadily growing number of studies exploring this therapeutic modality. Acupuncture is minimally invasive and associated with a lower potential for side effects as compared to conventional pharmacological interventions, in addition to being readily administered and associated with significant therapeutic efficacy in clinical trials[19-22]. In these trials, acupuncture has outperformed oral 5-aminosalicylic acid as a means of treating IBD[23], indicating that it is a feasible alternative therapy for the management of IBD. Acupuncture can also have effects on the function of both endogenous and exogenous MSC populations[24]. In one study, the combination of EA and tropomyosin receptor kinase B-transduced MSCs was associated with significantly better functional recovery following ischemic stroke[25], while in a separate study, combination treatment strategies led to better improvement in axonal regeneration, spinal cord conduction, and overall functional recovery following spinal cord injury[26], highlighting the promise of combining acupuncture and MSC therapy as an approach to managing these conditions. This review offers an overview of the therapeutic utility of combining acupuncture and MSC therapy as a means of managing IBD, with a particular focus on the potential synergistic interactions between these two therapeutic modalities, thereby providing a foundation for additional basic research and translational work in the clinic.

THE THERAPEUTIC PROMISE OF MSCS AS A TREATMENT FOR IBD
The pathogenesis of IBD

IBD is an autoimmune disease in which patients suffer from chronic intestinal inflammation and tissue damage due to the inappropriate activation of deleterious immune responses and associated immune cell infiltration[2] (Figure 1). While the precise pathogenesis of this disease is not fully understood, genetic, environmental, microecological, and immune factors are all believed to contribute to its etiology. The colonic lesions of patients with IBD present with elevated pro-inflammatory cytokine and chemokine levels[27], supporting a possible link between these factors and IBD progression. While early studies primarily focused on the roles that T helper type 1 cell (Th1) and Th2 populations play in IBD pathogenesis[28], Th17 cells have more recently been demonstrated to be critical for IBD onset[29], and interleukin (IL)-1 family cytokines are also central regulators of this process. IL-1β expression associated with macrophages and other innate immune cell populations is increased in the colonic mucosa of IBD patients[30]. Consistently, IL-18 levels are markedly elevated in the intestinal mucosa of patients with CD, leading to enhanced Th1 responses together with the disruption of normal T cell-derived cytokine secretion[31], altering the levels of factors including IL-6[32], IL-10[33], and IL-33[34], all of which are involved in IBD-related inflammatory responses. Chemokines are key mediators that guide the chemotactic migration of immune cells, with chemokines including CXC motif chemokine ligand 3 (CXCL3), CXCL6, and C-C motif chemokine ligand 28 being present at high levels in the colon in patients with IBD[35-37]. In addition to their modulatory effects on inflammatory and reparative responses, these chemokines are also vital for the maintenance of overall immunological homeostasis[38].

Figure 1
Figure 1 The pathogenesis of inflammatory bowel disease. In intestinal homeostasis state, the colonic epithelium is structurally intact, microorganisms are isolated from the intestine by the intestinal barrier, the body’s immune system is in a state of balance and the intestinal microenvironment is in a state of homeostasis. In the state of inflammatory bowel disease, the colonic epithelial structure is disrupted, the intestinal barrier is not functioning, microorganisms in the intestinal tract are exposed underneath the mucous membrane, and the expression of proinflammatory-related factors increases, thereby disrupting the immune balance and the homeostasis of the intestinal microenvironment. DC: Dendritic cell; Breg: Regulatory B cell; Th2: T helper type 2 cell; Treg: Regulatory T cell; ILC1: Type-1 innate lymphoid cell; ILC3: Type-3 innate lymphoid cell; Th17: T helper type 17 cell; Th9: T helper type 9 cell; Th1: T helper type 1 cell; NK: Natural killer.

Oxidative stress is also a key determinant of IBD pathogenesis[39]. The IBD-associated infiltration of the intestinal wall by inflammatory immune cells leads to the production of abundant reactive oxygen species (ROS) by neutrophils and macrophages[40]. Such ROS exposure adversely affects the normal homeostatic balance between oxidative and antioxidant responses in the intestines, culminating in the disruption of the tight junctions that exist between cells of the intestinal epithelium, thus impairing overall epithelial barrier function. Consistent with such a model, both IBD patients and animal models of colitis present with higher ROS levels in their colonic mucosa relative to healthy controls[41,42]. In early studies, IBD patients were also found to exhibit lower levels of the key antioxidant enzyme superoxide dismutase (SOD), consistent with greater oxidative stress[43]. IBD patients also reportedly present with lower serum total antioxidant capacity as compared to healthy controls[44], reaffirming the link between IBD development and the loss of systemic redox homeostasis. These reports thus underscore the central role that oxidative stress plays in the onset and/or progression of IBD.

Therapeutic functions of MSCs

MSCs are a widely distributed stem cell type that can be isolated from tissues including adipose tissue, bone marrow, endometrial polyps, menstrual blood, and even umbilical cord tissues. In addition to their accessibility, MSCs exhibit advantages including an excellent capacity for self-renewal and strong differentiation potential[45-48]. MSCs are capable of differentiating into a range of cell populations including both adipose and bone tissue cells[49]. MSCs also present with robust anti-inflammatory and immunomodulatory activities such that they are capable of suppressing the symptoms of various forms of inflammatory diseases, including IBD[50]. These beneficial effects of MSCs are mediated through their ability to modulate oxidative stress-related signaling, to suppress inflammation, and to promote tissue repair in a manner that can ultimately help curtail disease-related inflammation and oxidative stress. MSCs are also capable of protecting the intestinal nervous system and promoting intestinal barrier repair[51]. MSCs are thus ideal tools for the management of inflammatory diseases including IBD, as they exhibit a multifaceted array of therapeutic effects.

Antioxidant effects of MSCs

The nuclear factor-kappa B (NF-κB) and nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathways interact with one another to coordinate key transcriptional responses to inflammation and oxidative stress[52,53]. These factors are vital mediators of antioxidant processes (Table 1). The presence of H2O2 at micromolar concentrations, for instance, can activate NF-κB, while the antioxidant N-acetylcysteine can block this activation, emphasizing the close relationship between the activation of NF-κB signaling and oxidative stress[43]. Nrf2 is also closely related to oxidative stress, promoting the upregulation of heme oxygenase-1 (HO-1) and other factors that can respond to the loss of normal redox homeostasis[54]. Human umbilical cord MSC-derived exosome treatment was shown to protect against inflammation and oxidative stress induced by lipopolysaccharide and H2O2 treatment through the inhibition of Nrf2/NF-κB/nod-like receptor protein 3 (NLRP3) pathway activity within microglia[55]. These exosomes were found to upregulate Nrf2 while suppressing the phosphorylation of NF-κB p65 and the activation of the NLRP3 inflammasome in response to lipopolysaccharide. In a separate study, MSC transplantation in mice was found to help improve spinal cord injury outcomes, with the NF-κB pathway being related to the reparative mechanisms engaged following MSC transplantation[56]. In another study, knocking down Nrf2 was shown to weaken the antioxidant capacity of exosomes derived from MSCs in vitro and in vivo in mouse models of skin injury, supporting an important role for Nrf2 in this antioxidant pathway[57]. These findings indicate that MSCs are able to help alleviate oxidative stress in the context of disease through the regulation of the Nrf2 and NF-κB pathways.

Table 1 Antioxidant and anti-inflammatory mechanisms of mesenchymal stem cell.
Ref.
Model
Cell type
Method
Mechanism indicators
Pathway
Che et al[55]LPS-treated micehUC-MSCTail vein injectionTNF-α↓; IL-6↓; ROS↓; CD86↓; CD206↑; NLRP3↓; ASC↓; caspase-1↓Nrf2/NF-κB/NLRP3
Cao et al[56]SCI micehUC-MSCInjected along the spinal cordTNF-α↓; PTBP1↓TNF-α/NF-κB
Stavely et al[58]IBD miceBM-MSCEnemaIL-6↓; TNF↓; IL-1α↓; IL-1b↓; IFNG↓; CXCL2↓; TBX21↓; ITGAM↓; NOS2↓; ARG1↓; GATA3↓; MRC1↓; HMOX1↓; FOXP3↑; CD45↓-
Xian et al[146]SE miceMSC-ExoIntraventricular injection (in vivo), mix culture (in vitro)GFAP↓; C3↓; CD81↓; Ki67↓; TNF-α↓; IL-1β↓Nrf2/NF-κB
Xiao et al[147]ALI miceBM-MSCTail vein injectionIkbkb↓NF-κB/hedgehog
Zhang et al[148]IBD mice and CIA micehUC-MSCTail vein injectionTregs↑; Th17↓ETS2/AURKA/NF-κB/Fas/MCP-1
Li et al[149]ALI miceBM-MSCIn vitro MSC isolationTNF-α↓; IL-6↓; IL-10↓; HO-1↑; GPX-1↑Nrf2/ARE and NF-κB
Song et al[150]ADR induced nephropathy miceBM-MSCTail vein injectionMDA↓; IL-10↓; IFN-γ↓; TNF-α↓; IL-12↓; COX-2↓NF-κB
Han et al[151]SAH ratsBM-MSCTail vein injectionTGFβ↑; iNOS↓; CD16↓; CD11b↓; IL-1β↓; p-AMPK↑AMPK/NF-κB
Wang et al[152]SCI ratsMSC-ExoIntrathecal injectionTNF-α↓; IL-1β↓; IL-6; Bcl2↓; Bax↓; caspase-3↓miR-146b/TLR4/NF-κB p65

The antioxidant benefits of MSCs were also recently shown to contribute to the neuroprotective benefits of these cells[58], as demonstrated by their ability to protect against oxidative stress and neuronal damage in mouse intestinal organotypic cultures. These antioxidant effects were also validated in a mouse model of IBD, underscoring the direct ability of MSCs to shield intestinal neurons from the damaging effects of oxidative stress. While the authors of that study did not clarify the mechanisms underlying these therapeutic benefits, their findings nonetheless attest to the ability of MSCs to potentially counteract the oxidative stress characteristic of IBD development.

Anti-inflammatory effects of MSCs

Cytokines secreted by Th1, Th2, and Th17 cells are thought to be key mediators of IBD pathogenesis[28,29], including tumor necrosis factor-alpha (TNF-α), interferon-gamma (IFN-γ), IL-2, IL-17, IL-10, and transforming growth factor-beta. The presence of elevated intestinal levels of these factors can contribute to inflammatory and autoimmune response induction[59,60], thereby compromising intestinal integrity. Through their robust immunoregulatory effects, MSCs can migrate to sites of intestinal damage and restore local homeostasis, leading to the repair of IBD-related pathological changes. Several studies have demonstrated the ability of MSCs to employ a range of mechanisms to exert their anti-inflammatory effects (Table 1). For example, MSCs can inhibit effector T cell activity while inducing more robust regulatory T cell (Treg) responses[61,62], interacting with dendritic cells (DCs)[63], and interacting with natural killer (NK) cells[64], thereby shaping immune response characteristics.

MSCs can suppress CD3, TNF-α, and IL-2 activity by secreting prostaglandin E2 (PGE2) and thereby suppressing inflammation and related immune activity, contributing to the relief of colitis[65]. MSCs derived from adipose tissue have been shown to suppress the activation of Th1 cells, while MSC-derived IL-10 was found to induce Tregs involved in the therapeutic benefits of such treatment in the context of IBD[50]. MSCs are also capable of limiting the proliferation and Th17 differentiation of CD4 T cells, resulting in reduced IL-17, IL-22, IFN-γ, and TNF-α production. MSCs can inhibit the activation of Th1 cells while favoring higher levels of IL-4 release and inducing the function of Th2 cells[66], consistent with a model wherein these cells may achieve a net anti-inflammatory effect by respectively suppressing and enhancing pro-inflammatory and anti-inflammatory activities.

MSCs are capable of interacting with DCs[63]. For instance, one report found that MSCs were able to induce DC differentiation into regulatory DCs as a means of protecting against pathological outcomes in a dextran sodium sulfate (DSS)-induced mouse model of colitis, leading to improved colon length, body weight, and survival[60]. MSC-derived IL-10 and transforming growth factor-beta may act on DCs, thereby suppressing their maturation and indirectly altering T cell responses, resulting in a shift in the DC activity profile towards one favoring anti-inflammatory effects[67].

Interactions between MSCs and NK cells, which are key cytotoxic effector cells often linked to antitumor immunity, are also important immunomodulatory processes. NK cells achieve their cytotoxic effects by producing inflammatory factors including TNF-α and IFN-γ, playing a role in IBD pathogenesis[64]. MSCs are able to down-regulate the release of these pro-inflammatory factors from NK cells, thereby modulating the extent of the immune response. In addition to this, MSCs can also reduce the proliferation of NK cells in a manner that does not require contact between the cells; this process is inhibited by down-regulation of IFN-γ, which is affected by the release of various soluble factors, such as indoleamine 2,3-dioxygenase (IDO) and PGE2[64,68,69]. It is noteworthy that these factors involved in the interaction between MSC and NK cells are not only involved in modulation of anti-inflammatory effects mediated by MSC and NK cell crosstalk but are also able to regulate macrophages and increase the proportion of Tregs, thus ameliorating inflammation caused by factors such as PGE2, IDO, and nitric oxide[70,71]. It has been found that adipose-derived MSCs could modulate the M1 macrophage population by promoting the secretion of PGE2, thereby reducing inflammation in mice with colitis[72]. Furthermore, a further study on MSCs in mice showed that secretion of PGE2 increased the number of Tregs, leading to the alleviation of DSS-induced colitis[73], while another investigation demonstrated that human umbilical cord-derived MSC-mediated regulation of PGE2 and IDO levels increased Treg differentiation and enhanced the therapeutic effects of human umbilical cord blood MSC on DSS-induced colitis[74].

Restorative effects of MSC

The ability of MSCs to home to injured tissues in response to chemokines including CXCL12, CXCL4, and CXCL7 is closely related to their therapeutic benefits[75,76], with MSCs ultimately initiating their reparative programs after undergoing appropriate migration to sites of tissue damage.

MSCs can promote intestinal epithelial cell (IEC) proliferation while suppressing the apoptotic death of these cells, thereby helping mice recover normal intestinal structural and functional characteristics[77]. In one report focused on radiation-induced intestinal injury in mice that underwent human umbilical cord neural stem cell transplantation, these MSCs were able to engage in adipogenic and osteogenic differentiation, restore intestinal integrity, and promote functional recovery. In another study, bone marrow MSC treatment was able to suppress apoptotic cell death in a mouse model of necrotizing enterocolitis, significantly improving intestinal healing[78]. Studies have shown that conditioned medium derived from MSCs can promote IEC proliferation in the context of DSS- or trinitrobenzene sulfonic acid-induced colitis through the activation of phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) signaling[79]. Another report yielded similar results[9], with both in vitro and in vivo data indicating that DSS-induced colitis model animals experienced better colonic integrity and function following human embryo-derived MSC, with these effects being mediated by the insulin-like growth factor 1 (IGF-1)/PI3K/AKT pathway. The ability of MSCs to promote the proliferation of IECs is thus an important mechanism involved in the restoration of intestinal function and morphology. The miR-181a-containing exosomes derived from MSCs can also reportedly promote zonula occludens-1 (ZO-1) and claudin-1 upregulation, ultimately helping to restore the function and morphology of the intestinal barrier[80]. SOD3-transduced MSCs have recently been shown to target TNF-α as a means of restoring reductions in tight junction-associated protein levels in the TNF-α-induced intestinal epithelium, thereby facilitating intestinal repair. ZO-1 is important as a mediator of intestinal repair[81,82], supporting the maintenance of tight junctions between IECs. Claudin-1 is similarly important for the preservation and restoration of the intestinal barrier, inducing the proliferation and differentiation of the colonic epithelium[83,84], thereby preserving intestinal barrier integrity. ZO-1 and claudin-1 are thus key tight junction proteins relevant to colonic mucosal repair. In another study, MSCs were similarly found to effectively control tight junction proteins and to suppress apoptotic death in the context of colitis, contributing to improvements in intestinal morphology and function[64]. These results suggest that MSCs can effectively help repair damage to the intestinal barrier associated with the pathogenesis of IBD.

ACUPUNCTURE EXERTS ANTIOXIDANT AND ANTI-INFLAMMATORY EFFECTS TO TREAT IBD
Anti-inflammatory effects of acupuncture

Acupuncture exhibits robust anti-inflammatory activity (Table 2), downregulating inflammatory cytokine levels and inducing anti-inflammatory factor production in a manner similar to the effects of MSC treatment, thus allowing for the acupuncture-mediated relief of IBD. One meta-analysis of the acupuncture-based treatment of colitis determined that acupuncture was capable of downregulating TNF-α and IL-8 while promoting IL-10 upregulation, ultimately limiting inflammatory activity[85]. EA is capable of suppressing the activation of macrophages and the expression of IL-1β and inducible nitric oxide synthase, thus achieving anti-inflammatory effects[86]. Acupuncture can also modulate the Th17 to Treg ratio in IBD, decreasing CD3/CD8/IL-17-positive Th17 cell counts in splenic lymph nodes while increasing CD4/CD25/FoxP3-positive Treg numbers in mice[87]. Acupuncture can similarly help maintain appropriate Th1/Th2 and M1/M2 ratios[88,89]. ST36 EA can suppress NLRP3 and caspase-1 activation in a DSS-induced murine model of colitis, protecting against NLRP3/IL-1β pathway-associated inflammatory activity[90]. In contrast to its immunomodulatory effects in IBD.

Table 2 Antioxidant and anti-inflammatory mechanisms of acupuncture.
Ref.
Model
Intervention
Acupoints
Acupoint stimulation parameters
Mechanism indicators
Pathway
Zhang et al[86]IBD miceEABilateral: BL25EA: 2 Hz, 1 mA, 30 minutes, 7 daysIL-1β↓; iNOS↓; CD68↓-
Song et al[90]UC miceEAST36EA1: 100 Hz, 1 mA, 30 minutes, 7 days; EA2: 10 Hz, 1 mA, 30 minutes, 7 daysIL-1β↓; IL-6↓; IL-12↓; TNF-α↓; IL-17↓; IL-10↑-
Zhou et al[95]PTSD miceEAPretreatmentEA: 2/15 Hz, 1 mA, 30 minutes, 7 daysBDNF↓; AMPK↓; HO-1↓AMPK/Nrf2; Keap1/Nrf2
Yu et al[96]ALI rabbitsEABilateral: ST36; BL13EA1: 2/15 Hz, ≤ 1 mA, 15 minutes, 5 days; EA2: 2/15 Hz, ≤ 1 mA, 6 hours, 1 daysMDA↓; SOD↑; GPX↑; TNF-α↓; IL-6↓; HO-1↑Nrf2/ARE
Dai et al[153]SCI miceEABilateral: ST36; SP6EA: 60 Hz for 1.05 seconds and 2 Hz for 2.85 seconds, alternately; ≤ 5 μAApoE↑; TNF-α↓; IL-6↓; IL-1β↓; IL-10↑; TGF-β↑Nrf2-HO-1; Nrf2/NQO1/HO-1
Li et al[154]CIRI ratsEAGV20, SP6, bilateral: ST36EA: 2/15 Hz, 5 mA or 10 mA, 30 minutes, 5 daysTNF-α↓; HO-1↑; iNOS↓Nrf2/HO-1
Wang et al[155]VD miceAcupunctureGV20, bilateral: ST3610 minutes needle retentionTNF-α↓; TLR4↓; IL-6↓MyD88/NF-κB
Lou et al[156]I/R ratsEAPretreatment: ST36; SP6EA: 2/15 Hz, 1 mATNF-α↓; IL-1↓; IL-6↓; MPO↓; TLR4↓; p-NF-κB↓TLR4/NF-κB
Wu et al[157]UC ratsEA and HPMEA: Bilateral ST25. HPM: (Qihai)RN6; bilateral (Tianshu)ST25EA: 2 Hz, 4 mA, 20 minutes, 14 days; HPM: Moxa cones (refined mugwort floss)IL-1β↓; IL-6↓-
Liu et al[158]UC miceEABilateral: ST36EA: 2 Hz, 1 mA, 15 minutes, 7 daysIFN-γ↓; IL-6↓; TNF-α↓TLR4/MyD88
Antioxidant effects of acupuncture

Acupuncture exhibits significant antioxidant activity (Table 2). SOD, glutathione peroxidase (GPX), and catalase (CAT) are all endogenous antioxidant mediators, while malondialdehyde (MDA) concentrations are positively correlated with oxidative stress levels[91,92]. In one meta-analysis, acupuncture was shown to significantly decrease levels of MDA while increasing SOD, GPX, and CAT levels[93]. In a rat model of acute pancreatitis, EA treatment was associated with decreased histopathological scores in colon tissue together with significant decreases in myeloperoxidase and MDA levels, and a significant increase in serum IL-10 levels[94]. Experimental studies suggest that EA pretreatment can enhance hippocampal Nrf2, HO-1, and brain-derived neurotrophic factor expression in rats subjected to enhanced single prolonged stress-induced post-traumatic stress disorder, together with AMP-activated protein kinase phosphorylation, indicating that EA may exert its antioxidant effects via the Kelch-like ECH-associated protein 1/Nrf2 pathway[95]. In another study, EA treatment of the Zusanli (ST36) acupoint was able to reduce blood TNF-α and IL-6 levels while increasing SOD, GPX, and CAT levels and significantly increasing HO-1 and Nrf2 levels, consistent with the ability of EA to activate the Nrf2/antioxidant response element pathway to protect against oxidative stress-related tissue damage[96]. Acupuncture can also exert its antioxidant effects via the p38 mitogen-activated protein kinases/NF-κB pathway. The acupuncture treatment of the Zusanli (ST36), Baihui (GV20), and Taixi (KI3) acupoints, for example, can reduce p38 mitogen-activated protein kinases levels to suppress inflammation in the central nervous system[97]. Acupuncture at Zusanli (ST36) can also reportedly suppress nuclear NF-κB translocation and TP53 expression in a multiple cerebral infarction model system, while acupuncture at the Baihui (GV20), Yintang (EX-HN3), and Shuigou (GV26) acupoints was sufficient to reduce the deposition of β-secretase 1 controlled by NF-κB in APP/PS1 transgenic mice[98]. Acupuncture is also capable of exerting antioxidant effects to limit ROS biogenesis and prevent the apoptotic death of neurons[99].

Restorative effects of acupuncture

The effects of acupuncture in the context of IBD are not solely related to the modulation of pro- and anti-inflammatory mediator production, as it can also markedly affect intestinal barrier integrity and tissue function through the control of cellular apoptosis and the promotion of epithelial cell regeneration. Signaling via the PI3K/AKT axis is important for IEC proliferation, and activation of this pathway can improve intestinal integrity[9,79]. Acupuncture has been shown to activate PI3K/AKT signaling, controlling the Bcl-2/Bax and thereby inhibiting apoptotic cell death owing to the enhancement of anti-apoptotic signaling[100]. EA can also promote IGF-1 release and IGF-1/PI3K/AKT pathway activation[101]. The tight junctions that exist between IECs are vital for the maintenance of the integrity of the intestinal barrier. In a clinical trial in which CD patients were treated with acupuncture and moxibustion[102], analyses of intestinal morphology and ultrastructural features revealed significant improvements after treatment relative to pre-treatment findings. This included significant increases in the levels of proteins associated with tight junctions (ZO-1 and claudin-1), consistent with the ability of combined acupuncture and moxibustion treatment to restore the integrity of tight junctions and of the epithelium as a whole. In a separate study of colitis model mice[103], following EA treatment there were significant increases in claudin-1 and occludin protein levels in epithelial cells. When treating intestinal disorders other than IBD such as irritable bowel syndrome, acupuncture has also been shown to promote the upregulation of tight junction proteins including occludin, ZO-1, and claudin-1, thus helping to restore the integrity of intestinal structures while exerting anti-inflammatory benefits[104]. The mechanisms of action for MSCs and acupuncture are thus similar, with both being able to repair damaged intestinal barriers through the improvement of apoptotic cell death and the restoration of tight junction integrity, ultimately facilitating improvements in tissue repair and recovery in the context of IBD and other forms of intestinal injury.

Synergistic mechanisms of combined acupuncture and MSCs therapy in IBD treatment

The synergistic effects of combined acupuncture and MSCs therapy in IBD may involve multi-level immunomodulation and tissue repair. Acupuncture activates the vagus nerve-cholinergic anti-inflammatory pathway, suppressing the release of pro-inflammatory cytokines (e.g., IL-6, TNF-α) in the spleen and mesenteric lymph nodes while enhancing MSC proliferation. This process further modulates MSC secretion of anti-inflammatory mediators such as IL-10, thereby restoring intestinal immune homeostasis.

Furthermore, the combination therapy exhibits dual antioxidant potentiation. Acupuncture stimulation significantly reduces myeloperoxidase and MDA levels, whereas MSCs mitigate oxidative stress by inhibiting the Nrf2/NF-κB/NLRP3 signaling pathway. Concurrently, acupuncture activates the PI3K/AKT axis to promote intestinal barrier integrity restoration. Upon homing to damaged intestinal mucosa, MSCs initiate reparative functions by stimulating IEC proliferation. These findings collectively demonstrate that the multi-targeted reparative capacities of acupuncture combined with MSC therapy ensure structural reconstruction of the intestinal barrier.

MECHANISMS THROUGH WHICH COMBINING ACUPUNCTURE AND MSCS ACHIEVES BETTER THERAPEUTIC OUTCOMES
Acupuncture induces the homing of MSCs

The ability of MSCs to home to sites of damage represents a unique therapeutic advantage, and can be broadly classified into both systemic and non-systemic forms of homing[105]. In cases of systemic homing, administered or endogenous MSCs accumulate in the bloodstream and then progress through the stages of tethering and rolling, activation, arrest, transmigration or diapedesis, and migration, thereby ultimately migrating into sites of local tissue injury. In cases of non-systemic migration, MSCS transplanted into target tissues can be guided to injured sites through the effects of chemokines and other chemotactic stimuli[106]. These homing effects are crucial to the efficacy of MSC therapy, and some imaging studies have suggested that approaches that entail systemic MSC administration are associated with lower levels of homing efficiency[107,108], underscoring the need for further efforts to enhance homing efficiency as a means of achieving more efficacious MSC therapy. Current studies have sought to improve MSC homing through strategies including magnetic guidance[109], genetic modification[110], cell surface engineering[111], in vitro culture[112], and target tissue modification[113]. The majority of these strategies primarily aim to bolster systemic homing activity, but some, including magnetic guidance, instead focus on the improvement of non-systemic homing. Despite the promising results yielded by these studies, there remains a persistent need to design safer and more effective means of improving MSC homing efficiency. Current evidence suggests that the expression of stroma cell-derived factor (SDF)-1 on endothelial cells is vital for the activation of MSC homing[114]. SDF-1 is a C-X-C chemokine receptor type 4 (CXCR4) ligand, and this receptor is expressed on MSC surfaces[115-117]. MSCs additionally express the chemokine receptors CC Chemokine receptor 1 (CCR1), CCR4, CCR7, CCR9, CCR10, CXCR5, and CXCR6[116], although their functional roles will require further clarification. In one study, the co-expression of CXCR4 and CXCR7 was observed on bone marrow-derived MSCs (BMSCs), with these receptors cooperating together to promote the migration of these BMSCs[118], supporting a potential role for multiple chemokine receptors in this migratory process.

Acupuncture can activate signaling via the SDF-1/CXCR4 axis. One study found that in a mouse model of myocardial infarction[119], EA treatment of the neiguan (PC6) and xinshu (BL15) acupoints resulted in CXCR4 upregulation and corresponding improvements in myocardial pathogenesis. This supports the ability of EA to promote the mobilization of stem cells and to protect against myocardial damage via this SDF-1/CXCR4 pathway. Separately, the EA treatment of a rat model of myocardial infarction was shown to induce significant CXCR4 and SDF-1 upregulation[120], suggesting that this SDF-1/CXCR4 axis is an important mechanism through which acupuncture can promote tissue repair (Figure 2).

Figure 2
Figure 2 Schematic diagram of the synergistic mechanism between acupuncture and mesenchymal stem cells. Acupuncture can enhance the efficiency of exogenous mesenchymal stem cell (MSC) transplantation, thereby promoting their more effective arrival at the damaged colonic site. Concurrently, acupuncture can also promote the release of endogenous MSCs and increase the expression of the C-X-C chemokine receptor type 4 receptor on MSCs. As the expression of stroma cell-derived factor 1 in the peripheral blood circulation increases, the stroma cell-derived factor 1/C-X-C chemokine receptor type 4 pathway is activated, enhancing the homing ability of MSCs. Upon arrival near the damaged colonic tissue, MSCs improve intestinal injury through anti-inflammatory, antioxidant, and repair mechanisms. In the process of acupuncture synergizing with MSCs, acupuncture can also directly influence changes in the local microenvironment of the injury. Therefore, the combination of acupuncture and MSC transplantation improves the symptoms of inflammatory bowel disease. MSCs: Mesenchymal stem cells; SDF-1: Stroma cell-derived factor 1; CXCR4: C-X-C chemokine receptor type 4.

Combining EA and BMSC therapy through efforts to target the SDF-1/CXCR4 pathway can effectively treat intrauterine adhesions in a rat model system, leading to significant reductions in levels of endometrial fibrosis and pro-inflammatory cytokine levels as compared to the BMSC monotherapy or model groups[121]. This indicates that acupuncture can be combined with BMSC treatment as a means of improving BMSC transplantation efficiency through this SDF-1/CXCR4 pathway. Consistent with such a model[122], combined EA and MSC treatment was associated with better outcomes than either therapy alone in a rat ischemia/reperfusion (I/R) model, with corresponding increases in SDF-1 and CXCR4 mRNA levels.

Current research highlights three primary mechanisms through which acupuncture exerts its therapeutic effects in synergy with MSC therapy: (1) Acupuncture promotes MSCs to secrete growth factors, such as epidermal growth factor, which modulate cellular proliferation in peri-lesional tissues; (2) The combinatorial therapy amplifies SDF-1 expression in damaged tissues, thereby enhancing MSC chemotaxis. Experimental evidence demonstrates that EA adjuvant therapy upregulates both SDF-1 and its receptor CXCR4, establishing a chemotactic gradient that directs MSC migration to injury sites. This targeted homing mechanism is critical for localized tissue regeneration and functional recovery; and (3) Acupuncture synergizes with MSC therapy to suppress pro-inflammatory signaling pathways. Both EA and MSC transplantation independently reduce NF-κB activation and downstream inflammatory mediators, including IL-6 and TNF-α. Notably, their combined use results in a more pronounced anti-inflammatory response, as evidenced by significantly attenuated cytokine levels and histopathological inflammation in preclinical models.

Acupuncture promotes the proliferation and differentiation of MSCs

The use of acupuncture together with MSC transplantation has, to date, been used to manage central nervous system diseases including traumatic brain injury, spinal cord injury, and stroke[25,123,124], in addition to having been used to manage endometrial lesions and intestinal I/R injury[121,122]. This combination treatment strategy has been demonstrated to exhibit promising efficacy. Following combined EA and BMSC treatment of a rat model of intrauterine adhesions, improved endometrial morphology was observed in the combination treatment group relative to rats treated with EA or BMSCs alone. In an experimental rat model of spinal cord injury, the combination of governor vessel EA and MSC transplantation was found to promote effective recovery, with the researchers positing that governor vessel EA may be capable of activating metabolic activity in cells and initiating the production and release of endogenous neurotrophic factors within the local lesion microenvironment[125]. Similarly enhanced efficacy has also been observed in a rat I/R injury model system in response to combination treatment. Studies have demonstrated that after transecting the T10 spinal cord segment of healthy Sprague-Dawley rats and injecting a pre-cultured MSC suspension into the lesion site, EA combined with MSC transplantation significantly enhanced therapeutic outcomes[126]. The results revealed that EA promoted the expression of neurotrophin-3 in the injured spinal cord while markedly improving the differentiation capacity of transplanted MSCs into neuron-like or oligodendrocyte-like cells at the injury site. Concurrently, the survival rate of MSCs in the EA + MSC group was significantly higher compared to MSC monotherapy. Furthermore, multiple independent experiments investigating EA combined with MSCs have consistently replicated these findings[127,128]. These results preliminarily validate that acupuncture synergizes with MSC therapy to enhance cellular differentiation potential.

In addition to promoting exogenous MSC differentiation, it can promote endogenous MSC proliferation. Studies in mice, rats, humans, and horses have demonstrated that macrophages and MSCs are released into the peripheral blood following acupuncture-mediated stimulation of certain acupoints including LI-11, LI-4, Du-14, and Du-20[129]. Acupuncture may thus provide an effective means of driving the release of MSCs and other reparative cells. In one report, EA was also found to mobilize endogenous MSCs into the peripheral circulation, with these cells differentiating in vitro to produce adipocytes, osteoblasts, chondrocytes, and neural-like cells[130]. EA is thus capable of promoting endogenous MSC proliferation and promoting reparative cell release, underscoring its potential utility as a means of managing IBD when combined with MSC treatment.

Studies published to date have demonstrated the ability of combining acupuncture and MSC therapy to effectively treat IBD, with acupuncture facilitating the enhancement of MSC proliferation, differentiation, and transplantation. Acupuncture induces the local release of SDF-1 at sites of injury and into the bloodstream, inducing CXCR4 expression on MSCs and thereby improving their homing and differentiation abilities. In addition to their individual benefits, combining MSCs with acupuncture may lead to superior improvements in the intestinal environment through the ability of acupuncture to stimulate and mobilize endogenous MSCs and other cells with reparative functions (Figure 3). Acupuncture is capable of directly improving the intestinal microenvironment and regulating inflammatory activity[85,86]. It may also enhance MSC responses, suppressing inflammation by directly enhancing Treg and IL-10 responses while suppressing the activation of macrophages so as to promote the repair of the intestinal mucosa and the nearby vasculature[131]. Acupuncture can thus improve the symptoms of IBD while also facilitating more effective MSC transplantation.

Figure 3
Figure 3 Mechanisms of acupuncture combined with mesenchymal stem cells in the treatment of inflammatory bowel disease. MSCs: Mesenchymal stem cells; SDF-1: Stroma cell-derived factor 1; CXCR4: C-X-C chemokine receptor type 4; NK: Natural killer; Treg: Regulatory T cell; DCs: Dendritic cells; Th17: T helper type 17 cell; IL: Interleukin; TNF: Tumor necrosis factor.

MSCs have emerged as increasingly promising tools for IBD treatment given their robust immunomodulatory, anti-inflammatory, and reparative functions. MSCs have been demonstrated to offer strong benefits when used to treat animal models of IBD[50,60,74], and there are several clinical cases highlighting the benefits of MSC-based IBD treatment, underscoring the safety and feasibility of using this as a short-term treatment strategy[132]. However, the limited migratory activity of MSCs is an important issue that can hamper their efficacy, particularly when they are delivered systemically. While there have been marked advances in efforts to improve MSC transplantation, many challenges remain, especially with respect to safety[106].

A review of the current literature revealed that acupuncture, as a form of traditional Chinese medicine, can achieve marked benefits when treating IBD[19-23], while also promoting the differentiation, proliferation, and transplantation of MSCs. Acupuncture has been performed in China for more than 3000 years[133], and it continues to be a versatile, effective, widely applicable therapeutic modality. A growing number of studies have probed the mechanisms through which acupuncture functions, with several reports demonstrating the analgesic, anti-inflammatory, and antidepressant effects of acupuncture treatment[134-137]. Acupuncture has achieved marked efficacy in both preclinical and clinical research efforts.

MSCs have been demonstrated to exert their therapeutic benefits when used to treat IBD as a result of their antioxidant, anti-inflammatory, and neurotrophic activities together with their ability to repair the intestinal barrier, and the same is also true with respect to the ability of acupuncture to treat IBD[85,97,99]. Combining MSCs with acupuncture may thus provide a synergistic means of managing IBD. A review of the literature further revealed that EA stimulation can directly influence MSC differentiation and trigger endogenous MSC release in vivo[24]. Notably, EA can enhance MSC homing via the SDF-1/CXCR4 axis[122], indicating that acupuncture is a feasible approach to improving the efficiency of MSC transplantation. Additional information of interest found during the literature review when compiling this article included the observation that in certain malignancies, direct MSC transplantation can lead to negative effects, with MSCs associated with a potential risk of tumor differentiation or metastatic disease[138,139], thus potentially endangering patients. Acupuncture has been shown to enhance the cytotoxicity of NK and CD8 T cells in diseases characterized by immunosuppression, highlighting the unique bidirectional regulatory and immunomodulatory effects of this traditional treatment strategy[140,141]. This suggests that acupuncture, given its ability to reduce immunosuppression, may exert antitumor effects. This also raises the question of whether acupuncture is capable of counteracting the ability of MSCs to partially promote tumor growth and enhance MSC homing, allowing for combination treatment. Further work aimed at answering this question should be prioritized in the future.

Jin et al[142] recently demonstrated that the area postrema (AP) and caudal nucleus of the solitary tract (NST) transmit information related to inflammatory responses to the brain, with caudal NST silencing in mice contributing to unrestrained inflammation whereas neuronal activation was able to effectively regulate inflammatory activity. This suggests that the NST and AP in the brain are closely related to inflammation. Efforts to target the gastric and zusanli (ST36) neuronal cell groups have previously indicated that neurons labeled following ST36 acupuncture can project to the NST and AP[143], suggesting that acupuncture may help treat autoimmune diseases like IBD through its ability to impact this body-brain circuit. This provides additional support for a model in which acupuncture may lead to better efficacy in the context of stem cell therapy. Acupuncture is widely regarded as safe[20,144,145], making it an ideal component of therapeutic regimens for some patients who are unable to tolerate the side effects of certain drugs or are concerned about treatment-related risks. Combining acupuncture and MSCs is thus an attractive approach to IBD treatment. However, there remains a pressing need for additional studies seeking to clarify precisely how acupuncture can simultaneously regulate MSCs and local damage in the context of treatment.

CONCLUSION

MSCs have emerged as increasingly promising tools for IBD treatment given their robust immunomodulatory, anti-inflammatory, and reparative functions. MSCs have been demonstrated to offer strong benefits when used to treat animal models of IBD[50,61,76], and there are several clinical cases highlighting the benefits of MSC-based IBD treatment, underscoring the safety and feasibility of using this as a short-term treatment strategy[136]. However, the limited migratory activity of MSCs is an important issue that can hamper their efficacy, particularly when they are delivered systemically. While there have been marked advances in efforts to improve MSC transplantation, many challenges remain, especially with respect to safety[110].

ACKNOWLEDGEMENTS

The authors wish to acknowledge Xing-Fang Pan, Professor of China, University of Tianjin University of Traditional Chinese Medicine, for her help in revising the review.

Footnotes

Provenance and peer review: Unsolicited article; Externally peer reviewed.

Peer-review model: Single blind

Specialty type: Cell and tissue engineering

Country of origin: China

Peer-review report’s classification

Scientific Quality: Grade A, Grade B

Novelty: Grade B, Grade B

Creativity or Innovation: Grade B, Grade B

Scientific Significance: Grade B, Grade C

P-Reviewer: He Y; Tawil B S-Editor: Wang JJ L-Editor: A P-Editor: Zhang XD

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