• Lornoxicam (LOR)
• Silent information regulator-1
• design expert
• histopathological examination
• novasomes (Novas)
• ulcerative colitis

• active targeting
• drug delivery system
• inflammatory bowel diseases
• nanoparticles
• passive targeting
• targeted delivery

• Humans
• Inflammatory Bowel Diseases/drug therapy
• Nanoparticles/chemistry
• Drug Delivery Systems
• Animals
• Drug Carriers/chemistry
• Nanoparticle Drug Delivery System/chemistry
• Nanomedicine

• study was supported by Science and Technology Department of Jilin Province

• anti-inflammation
• butyrate
• inflammatory bowel disease
• magnolol
• polymer nanoparticles

• Animals
• Mice
• Polymers/pharmacology
• Butyrates/metabolism
• Butyrates/pharmacology
• Inflammatory Bowel Diseases/drug therapy
• Intestinal Mucosa
• Colon/metabolism
• Colitis/metabolism
• Disease Models, Animal

• Lactobacillus
• biotherapeutics
• designer probiotics
• genetic engineering
• gut microbiota

• Humans
• Probiotics/therapeutic use
• Probiotics/metabolism
• Genetic Engineering
• Biotechnology
• Gene Regulatory Networks

• Science and Engineering Research Board, Government of India under the Early Carrier Research Award (No. ECR/2017/000270) Grant
• 61/04/2022-IMM.BMS Indian Council of Medical Research, India

• extracellular vesicles
• galactose
• inflammatory bowel disease
• interleukin 10
• oral protein administration

• Mice
• Animals
• Cytokines
• Interleukin-10
• Inflammatory Bowel Diseases/drug therapy
• Inflammatory Bowel Diseases/metabolism
• Extracellular Vesicles/metabolism
• Chitosan
• Hydrogels
• Mammals

• 32071384 National Natural Science Foundation of China
• 2021YFC2102300 National Key Research and Development Program

• Astragalus membranaceus
• Astragalus membranaceus Extracts
• Crohn’s Disease
• Inflammatory Bowel Disease
• Preclinical Studies
• Ulcerative Colitis

• Humans
• Astragalus propinquus
• Inflammatory Bowel Diseases/drug therapy
• Colitis, Ulcerative/drug therapy
• Anti-Inflammatory Agents/therapeutic use
• Antioxidants

• ROS-related diseases
• antioxidant
• enzyme-mimic
• nanozymes
• oxidative stress

• the Medical Key Science Project of Shanxi Province
• the Scientific and Technological Activities for Overseas Students in Shanxi Province

• Immunotherapy
• gene delivery
• inflammatory bowel disease
• nanomedicines
• oral drug delivery
• siRNA

• Nrf-2/HO-1
• ROS scavenger
• colitis
• diselenide-bridged nanogel
• nano-antioxidant

• Mice
• Animals
• Antioxidants/pharmacology
• Antioxidants/therapeutic use
• Reactive Oxygen Species/metabolism
• Dextran Sulfate/adverse effects
• Hyaluronic Acid
• Colitis/chemically induced
• Colitis/drug therapy
• Inflammatory Bowel Diseases
• Disease Models, Animal

• ROS scavenging
• combination therapy
• gene interference
• inflammatory bowel disease
• mesoporous polydopamine nanoparticles

• Catechols/therapeutic use
• Humans
• Indoles
• Inflammatory Bowel Diseases/genetics
• Inflammatory Bowel Diseases/therapy
• Nanoparticles
• Polymers
• RNA, Small Interfering/genetics
• RNA, Small Interfering/therapeutic use
• Reactive Oxygen Species
• Tumor Necrosis Factor-alpha/genetics

• ischemia–reperfusion injuries
• nitroxide radicals
• oxidative stress
• reactive oxygen species
• redox nanoparticles

• Gut microbiota
• Intestinal barrier
• Lamina propria
• Mucosal Immunity
• Nanomedicine
• Oral immunotherapy
• Peyer’s patches

• Administration, Oral
• Anti-Inflammatory Agents/administration & dosage
• Anti-Inflammatory Agents/pharmacokinetics
• Gastrointestinal Microbiome/physiology
• Humans
• Immune Tolerance/physiology
• Immunity, Mucosal/physiology
• Intestinal Mucosa/physiology
• Mucous Membrane/metabolism
• Nanoparticle Drug Delivery System/pharmacokinetics
• Vaccines/administration & dosage

• R01 NS122536 NINDS NIH HHS
• R01 DK125087 NIDDK NIH HHS
• P30 DK034933 NIDDK NIH HHS
• R01 CA210273 NCI NIH HHS
• U01 CA210152 NCI NIH HHS
• R01 DK108901 NIDDK NIH HHS
• R01 AI127070 NIAID NIH HHS
• R01 DE030691 NIDCR NIH HHS

• Antibacterial
• Dysbiosis
• Restoring
• Targeting
• Toxicity

• fullerene
• immunity
• ulcerative colitis

• Inflammatory bowel disease
• Pharmacokinetics
• Poor-water soluble drug
• ROS
• Redox nanoparticles
• Silymarin

Colonic Drug Delivery Systems (CDDS) are especially advantageous for local treatment of inflammatory bowel diseases (IBD). Site-targeted drug release allows to obtain a high drug concentration in injured tissues and less systemic adverse effects, as consequence of less/null drug absorption in small intestine. This review focused on the reported contributions in the last four years to improve the effectiveness of treatments of inflammatory bowel diseases. The work concludes that there has been an increase in the development of CDDS in which pH, specific enzymes, reactive oxygen species (ROS), or a combination of all of these triggers the release. These delivery systems demonstrated a therapeutic improvement with fewer adverse effects. Future perspectives to the treatment of this disease include the elucidation of molecular basis of IBD diseases in order to design more specific treatments, and the performance of more in vivo assays to validate the specificity and stability of the obtained systems.

• colon
• drug delivery
• inflammatory bowel diseases
• intestinal permeability

• Boolean AND gate
• Designer probiotic
• Gut inflammation
• Nitrate sensing
• Thiosulfate sensing
• Whole cell biosensor

• Metabolic engineering
• Microbiome
• Probiotics
• Synthetic biology

• Clinical Trials as Topic
• Dysbiosis/therapy
• Gastrointestinal Microbiome
• Humans
• Inflammation/diagnosis
• Inflammation/therapy
• Inflammatory Bowel Diseases/diagnosis
• Inflammatory Bowel Diseases/therapy
• Metabolic Diseases/diagnosis
• Metabolic Diseases/therapy
• Metabolic Engineering
• Neoplasms/diagnosis
• Neoplasms/therapy
• Probiotics/therapeutic use
• Synthetic Biology

• 2018YFA0901800 The National Key Research and Development Program of China
• 2018YFA0901400 The National Key Research and Development Program of China
• 21908003, 21636001 The National Natural Science Foundation of China
• 21776008 The National Natural Science Foundation of China
• buctrc201911 The Fundamental Research Funds for the Central Universities
• 2019M650454 The China Postdoctoral Science Foundation

Crohn’s disease is a chronic inflammatory disorder of the gastrointestinal tract associated with abdominal pain and diarrhea. Pain caused by Crohn’s disease likely involves neurogenic inflammation which seems to involve the ion channel transient receptor potential ankyrin 1 (TRPA1). Since the promoter methylation of TRPA1 was shown to influence pain sensitivity, we asked if the expression of TRPA1 is dysregulated in patients suffering from Crohn’s disease.

The methylation rates of CpG dinucleotides in the TRPA1 promoter region were determined from DNA derived from whole blood samples of Crohn patients and healthy participants. Quantitative sensory testing was used to examine pain sensitivities.

Pressure pain thresholds were lower in Crohn patients as compared to healthy participants, and they were also lower in females than in males. They correlated inversely with the methylation rate at the CpG − 628 site of the TRPA1 promoter. This effect was more pronounced in female compared to male Crohn patients. Similar results were found for mechanical pain thresholds. Furthermore, age-dependent effects were detected. Whereas the CpG − 628 methylation rate declined with age in healthy participants, the methylation rate in Crohn patients increased. Pressure pain thresholds increased with age in both cohorts.

The TRPA1 promoter methylation appears to be dysregulated in patients suffering from Crohn’s disease, and this effect is most obvious when taking gender and age into account. As TRPA1 is regarded to be involved in pain caused by neurogenic inflammation, its aberrant expression may contribute to typical symptoms of Crohn’s disease.

• Crohn’s disease
• IBD
• Pressure pain
• Promoter methylation
• TRPA1

• Inflammatory bowel disease
• Janus-prodrug
• ROS-responsive
• Self-assembled
• Site-specific therapy

This study examines the dual role of Escherichia coli in the course of ulcerative colitis (UC). The intestinal microbiota is considered to play an important role in UC pathogenesis, but how E. coli contributes to inflammation in UC is still unknown. On the one hand, we demonstrated that there was a significant increase in the number of E. coli at the sites of inflammation in patients with UC, which can lead to immune system activation, whilst, on the other hand, E. coli may contribute to the resolution of inflammatory reactions since E. coli can inhibit hydroxyl radical formation by eliminating substrates of the Fenton reaction, by assimilating ferrous iron (Fe²⁺) and inducing the decomposition of hydrogen peroxide (H₂O₂). On this way, E. coli may affect the initiation and/or prolongation of remission stages of UC.

Ten E. coli strains were isolated from the colonic mucosa of patients in the acute phase of UC. Using PCR, we examined the presence of genes encoding catalases (katG and katE) and proteins participating in iron acquisition (feoB, fepA, fhuA, fecA, iroN, fyuA, and iutA) in these E. coli strains. To determine if iron ions influence the growth rate of E. coli and its ability to decompose H₂O₂, we grew E. coli in defined culture media without iron (M9(-)) or with ferrous ions (M9(Fe²⁺)). Expression levels of genes encoding catalases were examined by real-time PCR.

All investigated E. coli strains had catalase genes (katG, katE), genes coding for receptors for Fe²⁺ (feoB) and at least one of the genes responsible for iron acquisition related to siderophores (fepA, fhuA, fecA, iroN, fyuA, iutA). E. coli cultured in M9(Fe²⁺) grew faster than E. coli in M9(-). The presence of Fe²⁺ in the media contributed to the increased rate of H₂O₂ decomposition by E. coli and induced katG gene expression.

E. coli eliminates substrates of the Fenton reaction by assimilating Fe²⁺ and biosynthesizing enzymes that catalyze H₂O₂ decomposition. Thus, E. coli can inhibit hydroxyl radical formation, and affects the initiation and/or prolongation of remission stages of UC.

• Catalases
• Escherichia coli
• Ferrous acquisition
• Ulcerative colitis

• Air Pollutants/adverse effects
• Anti-Bacterial Agents/adverse effects
• Anti-Inflammatory Agents, Non-Steroidal/adverse effects
• Colitis, Ulcerative/diagnosis
• Colitis, Ulcerative/epidemiology
• Colitis, Ulcerative/therapy
• Crohn Disease/diagnosis
• Crohn Disease/epidemiology
• Crohn Disease/therapy
• Diet/adverse effects
• Environment
• Environmental Exposure/adverse effects
• Estrogens/adverse effects
• Humans
• Recurrence
• Risk Assessment
• Risk Factors
• Smoking/adverse effects
• Smoking/epidemiology
• Stress, Psychological/epidemiology
• Treatment Outcome

This study was aimed to investigate the beneficial effects of quercetin (QCT) against trinitrobenzene sulfonic acid (TNBS) induced clinical, morphological, and biochemical alterations in rats.

Colitis in rats was induced by administration of TNBS (25 mg dissolved in 0.25 ml of 30% ethanol) 8 cm into the rectum of the rat using a catheter. The animals were divided into six experimental groups (n = 6); naive (saline only without TNBS administration), control (saline + TNBS), standard (sulfasalazine 25 mg/kg + TNBS), QCT (25) (QCT 25 mg/kg + TNBS), QCT (50) (QCT 50 mg/kg + TNBS), QCT (100) (QCT 100 mg/kg + TNBS). Sulfasalazine (25 mg/kg) and QCT (25, 50 and 100 mg/kg) were administered per oral for 11 days and the colonic damage was evaluated in terms of macroscopical (body weight, stool consistency, rectal bleeding, and ulcer index) and biochemical parameters (myeloperoxidase activity, lipid peroxidation, nitrite, and glutathione).

Treatment with QCT (50, 100 mg/kg) for 10 days following TNBS administration significantly attenuated the clinical, morphological, and biochemical alterations induced by TNBS, whereas it was found to be not effective at its lower dose (25 mg/kg) throughout the experimental protocol.

QCT attenuates the clinical, morphological and biochemical alterations induced by TNBS possibly via its antioxidant mechanism.

• Inflammatory bowel disease
• myeloperoxidase
• oxidative stress
• ulcer index

Silica-containing redox nanoparticles act as adsorbents for peritoneal dialysis and orally administrable drug carriers for the treatment of gastrointestinal inflammation.

• Adult
• Aged
• CD4-Positive T-Lymphocytes/metabolism
• Chamomile/chemistry
• Charcoal/therapeutic use
• Coffee
• Colitis, Ulcerative/drug therapy
• Colitis, Ulcerative/immunology
• Female
• Flow Cytometry
• Humans
• Kinetics
• Male
• Mesalamine/therapeutic use
• Middle Aged
• Plant Extracts/therapeutic use
• Terpenes/chemistry
• Young Adult

• DNA damage
• ROS
• anthocyanins
• antioxidants
• bilberry
• encapsulation
• glutathione
• pectin
• whey protein

• Anthocyanins/administration & dosage
• Anthocyanins/pharmacology
• Antioxidants/administration & dosage
• Antioxidants/pharmacology
• Caco-2 Cells
• Capsules/chemistry
• DNA Damage/drug effects
• Fruit/chemistry
• Glutathione/metabolism
• Humans
• Malus
• Milk Proteins
• Oxidative Stress/drug effects
• Pectins
• Plant Extracts
• Reactive Oxygen Species/metabolism
• Vaccinium myrtillus/chemistry
• Whey Proteins

• anti-inflammation
• nitroxide radicals
• oxidative stress
• reactive oxygen species
• redox nanoparticles

This study investigated a possible role of Escherichia coli in propagation and perpetuation of the chronic inflammation in ulcerative colitis (UC). The lesions of UC are located superficially on the rectal and/or colonic mucosa. It is suggested that the commensal bacteria of the digestive tract may play a role in the pathogenesis of UC. Several studies have demonstrated proliferation of E. coli in the gut of UC patients. An increase in the number of E. coli in the inflamed tissue is most probably related to the abundance of iron ions produced by the bacteria.

Colon mucosal biopsies were collected from 30 patients with acute-phase UC, both from tissues with inflammatory changes (n = 30) and unchanged tissue with no inflammatory changes (n = 30) from the same patient. Biopsies were also taken from 16 patients with irritable bowel syndrome diarrhea who comprised the control group. Quantitative and qualitative analysis of the biopsy specimens was performed using culture methods and real-time polymerase chain reaction (PCR). Genotyping of the E. coli isolates was done using pulsed-field gel electrophoresis. Multiplex PCR was used to compare the E. coli strains for the presence of genes responsible for synthesis of iron acquisition proteins: iroN, iutA, iha, ireA, chuA, and hlyA.

We demonstrated that there was a significant increase in the number of E. coli at the sites of inflammation in patients with UC compared to the control group (P = 0.031). Comparative analysis of the restriction patterns of E. coli isolated from inflammatory and unchanged tissues showed that the local inflammatory changes did not promote specific E. coli strains. There was a significant difference in the frequency of the iroN gene in E. coli isolated from patients with UC as compared to the control group.

The increase in the numbers of E. coli in the inflammatory tissues is related to the presence of chuA and iutA genes, which facilitate iron acquisition during chronic intestinal inflammatory processes.

• Antioxidant status
• Gastro-protective effect
• Gastrointestinal disorders
• Mycophenolate mofetil
• Silymarin

Exacerbation of hypoxic injury after reoxygenation is a crucial mechanism mediating organ injury in transplantation, and in myocardial, hepatic, gastrointestinal, cerebral, renal, and other ischemic syndromes. The occlusion and reperfusion of the splanchnic artery is a useful animal model to elucidate the mechanism of gastrointestinal injury induced by ischemia-reperfusion (I/R). Although xanthine oxidase is a major source of reactive oxygen species (ROS), which plays an important role in the I/R-induced intestinal injury, there are many other sources of intracellular ROS. Various treatment modalities have been successfully applied to attenuate the I/R injury in animal models. This review focuses on the role of oxidant stress in the mechanism of I/R injury and the use of antioxidant agents for its treatment.

• antioxidant
• ischemia-reperfusion
• oxidant stress

AIM: To investigate the effects of the free radical scavenger bis(1-hydroxy-2,2,6,6-tetramethyl-4-piperidinyl)decandioate (IAC) in the dextran sodium sulphate (DSS) experimental model of ulcerative colitis.

METHODS: Colitis was induced in Sprague Dawley male rats by administration of 5% DSS in drinking water. IAC (30 mg/kg, lipophilic or hydrophilic form) was administered daily (orally or ip) for 6 d until sacrifice. Colonic damage was assessed by means of indirect (Disease Activity Index score) and direct measures (macroscopic and microscopic scores) and myeloperoxidase (MPO) activity. Neutrophil infiltration within the tissue and glutathione S-transferase activity were also investigated.

RESULTS: DSS-induced colitis impaired body weight gain and markedly increased all inflammatory parameters. Six-day treatment with lipophilic IAC significantly reduced intestinal damage caused by inflammation, induced a down-regulation in MPO activity (0.72 ± 0.12 and 0.45 ± 0.12 with lipophilic IAC po and ip, respectively, vs 1.10 ± 0.27 in untreated DSS colitis animals) and minimized DSS-induced neutrophil infiltration, while hydrophilic IAC administered orally did not ameliorate DSS-induced damage.

CONCLUSION: These results support the hypothesis that reactive oxygen metabolites contribute to inflammation and that the radical scavenger IAC has therapeutic potential in inflammatory bowel disease.

• Dextran sodium sulphate-induced colitis
• Oxidative damage
• Inflammatory bowel disease
• Bis(1-hydroxy-2,2,6,6-tetramethyl-4-piperidinyl)decandioate
• Radical scavenger
• Animal models