• Gang Li, Lei Chen, and Kai Chen.
• Department of Orthopaedics, Ward 2, The First Affiliated Hospital of the Medical College, Shihezi University, Shihezi, Xinjiang, China (mainland).
• Med. Sci. Monit. 2018 Jun 14; 24: 4064-4072.

AbstractBACKGROUND The aim of this study was to use a rat model of femoral fracture healing to study the effects of curcumin on cell autophagy, compared with treatment with 3-methyladenine (3-MA), an inhibitor of autophagy. MATERIAL AND METHODS Thirty-six Sprague-Dawley rats with right mid-femoral fracture were divided into three groups: the curcumin-treated group (N=12) (gavage with curcumin 400 mg/kg/day); the curcumin + 3-MA-treated group (gavage with curcumin 400 mg/kg/day + 3-MA 30 mg/kg/day); and the control group (N=12) (gavage normal saline). Each group underwent femoral bone imaging using anteroposterior X-ray and micro-computed tomography (CT) at two weeks and six weeks following bone fracture. All rats were euthanized at the end of the study. Histology of the bone was performed to compare bone healing. Immunofluorescence and immunohistochemical tissue staining and Western blots were performed, to compare the expression of autophagy-related proteins, Beclin-1 and LC3-II. RESULTS Autophagy of rat femoral bone tissue was activated following fracture, increasing with time, reaching a peak at 24 hours. Imaging and histology showed that curcumin promoted the fracture healing in rats, which was reduced by treatment with 3-MA. Immunohistochemistry, immunofluorescence, and Western blot showed that curcumin treatment increased the expression of Beclin-1 and LC3-II, which were reduced by treatment with the autophagy inhibitor, 3-MA. CONCLUSIONS The findings of this study, in a rat model of femoral bone fracture healing, showed that curcumin promoted bone healing and autophagy, which were reduced by treatment with 3-MA, a known inhibitor of autophagy.

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