ArticleIranian journal of basic medical sciences2026
Protective effects and mechanism of chrysophanol against age-related osteoporosis in rats.
Article in Iranian journal of basic medical sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Objectives: 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.
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