Protective effects and mechanism of chrysophanol against age-related osteoporosis in rats
نویسندگان
1 Department of Traditional Chinese Medicine, Suzhou City Xiangcheng District Third People’s Hospital, Suzhou 215100, China
2 Institute of Translational Medicine, Shanghai University, Shanghai 200444, China
3 Department of Traditional Chinese Medicine, Suzhou City Xiangcheng District Third People’s Hospital, Suzhou 215100, China
4 Department of Traditional Chinese Medicine, Suzhou City Xiangcheng District Third People’s Hospital, Suzhou 215100, China
5 Department of Traditional Chinese Medicine, Suzhou City Xiangcheng District Third People’s Hospital, Suzhou 215100, China
6 Institute of Translational Medicine, Shanghai University, Shanghai 200444, China
7 Institute of Translational Medicine, Shanghai University, Shanghai 200444, China
doi
10.22038/ijbms.2026.87322.18864چکیده
Objective(s): This study aimed to investigate the protective effect and underlying mechanism of chrysophanol (CPH) on senile osteoporosis (OP) in rats. Materials and Methods: Twenty-four-month-old rats were divided into an aged OP model group and low- (10 mg/kg), medium- (20 mg/kg), and high-dose (50 mg/kg) CPH groups, with eight-month-old rats used as the control group. After 60 days of oral CPH administration, the bone mineral density (BMD), bone volume fraction (BV/TV), trabecular number (TbN), and trabecular separation (TbSp) of the femur were analysed using Micro-CT. Serum levels of bone formation markers (alkaline phosphatase, ALP; osteocalcin, OC) and bone resorption markers (type I collagen crosslinked N-telopeptide, NTX; tartrate-resistant acid phosphatase, TRACP) were determined by ELISA. Pathological changes in the femur were observed via H&E staining, and the expression of p-AKT and p-mTOR proteins in bone marrow was detected by western blotting.Results: Compared with those in the control group, the bone formation marker levels, BMD, BV/TV, and TbN in the model group significantly decreased, whereas the bone resorption marker levels, TbSp, and expression levels of p-AKT and p-mTOR significantly increased, with obvious bone structure destruction. CPH treatment reversed these changes in a dose dependent manner, significantly enhanced bone formation, inhibited bone resorption, improved bone density and microstructure, and down-regulated the expression of p-AKT and p-mTOR. Conclusion: CPH can effectively improve bone density and microstructure in aged osteoporotic rats, and its bone-protective effect may be related to the inhibition of the PI3K/AKT/mTOR signaling pathway.
