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.