Published online Apr 15, 2024. doi: 10.4239/wjd.v15.i4.769
Peer-review started: December 31, 2023
First decision: January 16, 2024
Revised: January 22, 2024
Accepted: March 5, 2024
Article in press: March 5, 2024
Published online: April 15, 2024
Processing time: 102 Days and 17.6 Hours
Icariin (ICA) has multiple pharmacological activities. However, its effect on bone defect repair in the context of type 1 diabetes mellitus (T1DM) remains unclear.
ICA possesses the ability to promote osteogenesis and exert protective effects in T1DM. Therefore, ICA may have therapeutic potential for repairing bone defects in patients with T1DM.
To explore the role of ICA on bone defect repair in T1DM models.
The effects of ICA on osteogenesis and angiogenesis were evaluated by molecular biology techniques in vitro. After a T1DM rat model was established, we evaluated the effect of ICA on bone formation in a defect area.
ICA promoted bone marrow mesenchymal stem cell (BMSC) osteogenic differentiation and induced osteogenesis-angiogenesis coupling of BMSCs in vitro. Subsequently, we observed that ICA facilitated bone formation and type H vessel formation in the defect area of the T1DM rat model. Sequential fluorescent labeling confirmed that ICA could effectively accelerate the rate of bone formation in the defect area.
ICA accelerated bone regeneration by inducing osteogenesis-angiogenesis coupling of BMSCs in the T1DM rat model.
Our study highlighted the importance of effective coupling of osteogenesis and angiogenesis in bone regeneration in the context of T1DM.