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Updated: Apr 8, 2026
Murine Flexor Tendon Injury and Repair Surgery
Published on: September 19, 2016
Chitosan prevents adhesion during rabbit flexor tendon repair via the sirtuin 1 signaling pathway
Qiang Chen1, Hui Lu1, Hu Yang1
1Department of Hand Surgery, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang 310003, P.R. China.
Abstract:
Chitosan has been demonstrated to exert potent anti-adhesive activity during tendon repair; however, the underlying molecular mechanisms remain unclear. The present study aimed to investigate the preventive effects of chitosan on adhesion in rabbit tendon repair, and to investigate the role of the sirtuin (SIRT)1 signaling pathway in this process. A total of 30 rabbits were divided randomly into three equal groups: Group 1, saline treatment; group 2, chitosan treatment; and group 3, chitosan + nicotinamide treatment. The flexor tendon of each of the rabbits was injured, and subsequently each rabbit was injected with the one of the reagents. Six weeks post‑surgery, all of the rabbits were sacrificed and their flexor tendons were harvested for subsequent evaluation of adhesion. Western blotting was used to determine the protein expression levels of specific signaling molecules. An MTT assay was conducted to evaluate the viability of human tenocytes and flow cytometry was used to analyze the apoptotic rate of the cells. The present study demonstrated that treatment with chitosan relieved adhesion in the rabbits with flexor tendon injuries. In addition, chitosan treatment increased SIRT1 expression, and reduced acetylated p65 and p53 expression in the tendons. The effects of chitosan on the tendons were attenuated by treatment with nicotinamide (a SIRT1 inhibitor). In the human tenocytes, pretreatment with chitosan resulted in an inhibition of interleukin (IL)‑1β‑induced apoptosis. Furthermore, chitosan reversed the IL‑1β‑induced downregulation of SIRT1 and upregulation of acetylated p65 and p53. Furthermore, downregulation of Sirt1 by RNA interference abrogated the effects of chitosan on the levels of p65 and p53 acetylation, and the rate of tenocyte apoptosis. In conclusion, chitosan treatment prevented adhesion via the SIRT1 signaling pathway during rabbit flexor tendon repair. These results indicate that SIRT1 may be targeted for therapeutic intervention in flexor tendon injury.
Insights
Chitosan effectively prevents tendon adhesions by activating the sirtuin 1 (SIRT1) pathway, reducing inflammation and cell death. This discovery highlights SIRT1 as a potential therapeutic target for flexor tendon injuries.
Area of Science:
- Biomaterials Science
- Regenerative Medicine
- Molecular Biology
Background:
- Chitosan demonstrates anti-adhesive properties in tendon repair, but its molecular mechanisms are not fully understood.
- Adhesion formation after flexor tendon injury can impede functional recovery.
Purpose of the Study:
- To investigate the preventive effects of chitosan on adhesion in rabbit tendon repair.
- To elucidate the role of the sirtuin 1 (SIRT1) signaling pathway in chitosan's anti-adhesive mechanism.
Main Methods:
- Utilized a rabbit flexor tendon injury model with saline, chitosan, and chitosan + nicotinamide treatments.
- Assessed adhesion formation, protein expression (Western blotting), tenocyte viability (MTT assay), and apoptosis (flow cytometry).
- Investigated SIRT1 pathway involvement using a SIRT1 inhibitor (nicotinamide) and RNA interference.
Main Results:
- Chitosan treatment significantly reduced adhesion in rabbit flexor tendons.
- Chitosan increased SIRT1 expression and decreased acetylated p65 and p53 levels.
- Nicotinamide attenuated chitosan's anti-adhesive effects, confirming SIRT1 pathway involvement.
- In human tenocytes, chitosan inhibited IL-1β-induced apoptosis and modulated SIRT1, p65, and p53 acetylation.
Conclusions:
- Chitosan prevents tendon adhesion through the SIRT1 signaling pathway during flexor tendon repair.
- SIRT1 activation by chitosan offers a potential therapeutic strategy for managing flexor tendon injuries and preventing adhesions.
