人参皂苷Rh2通过OPG/RANKL信号通路介导对老年大鼠骨量流失的保护作用

目的观察人参皂苷Rh2对老年大鼠骨强度和骨量的影响,并探索可能的机制。方法 30只雌性Sprague Dawley大鼠随机分为3组:对照组(Con,10只3月龄大鼠);模型组(Mod,10只24月龄老年大鼠)及老年大鼠+人参皂苷Rh2治疗组(Rszg,大鼠每天接受300 mg/kg人参皂苷Rh2治疗12周)。12周后取双侧股骨进行微型计算机断层扫描(Micro-CT)、组织病理切片、骨生物力学以及蛋白质印迹(WB)检测。结果 Mod组大鼠的骨密度(BMD)、骨显微结构和最大载荷和弹性模量等指标均明显低于Con组(P0.05)。人参皂苷Rh2治疗后骨密度、骨显微结构、最大载荷和弹性模量等指标均有明显改善,差异有统计学意义(P0.05)。WB检测显示Mod组OPG和Runx2表达水平较Con组明显下调,而RANKL表达水平明显上调(P0.05)。Rszg组OPG和Runx2表达水平较Mod组明显上调,而RANKL表达水平显著下调。结论人参皂苷Rh2治疗可以显著改善老年大鼠股骨骨强度和骨量,而这种疗效可能通过OPG/RANKL信号通路来介导。

Protective effect of ginsenoside Rh2 on bone loss in aged rats mediated by OPG / RANKL signaling pathway

Objective To observe the effect of ginsenoside Rh2 on bone strength and bone mass in aged rats and explore possible mechanisms. Methods Thirty female Sprague Dawley rats were randomly divided into 3 groups: control group (Con, 10 3-month-old rats); model group (Mod, 10 24-month-old aged rats) and aged rats + ginsenoside Rh2 Group (Rszg, rats received 300 mg / kg ginsenoside Rh2 treatment for 12 weeks). After 12 weeks, bilateral femurs were taken and analyzed by micro-CT (Micro-CT), histopathological sections, bone biomechanics, and Western blot (WB) detection. Results The bone density (BMD), bone microstructure, maximum load and elastic modulus of the Mod group rats were significantly lower than those of the Con group (P <0.05). After treatment with ginsenoside Rh2, bone mineral density, bone microstructure, maximum load, and elastic modulus were significantly improved, which was statistically significant (P <0.05). WB detection showed that the expression levels of OPG and Runx2 in Mod group were significantly lower than those in Con group, while the expression levels of RANKL were significantly increased (P <0.05). The expression levels of OPG and Runx2 in the Rszg group were significantly increased compared with the Mod group, while the expression levels of RANKL were significantly decreased. Conclusions Ginsenoside Rh2 treatment can significantly improve femoral bone strength and bone mass in aged rats, and this effect may be mediated by the OPG / RANKL signaling pathway.