人参皂苷抗糖皮质激素诱发骨质疏松的效应及机制研究

Impact and Mechanism of Ginsenoside on anti-glucocorticoid Induced Osteoporosis

目的:研究人参皂苷(GSS)对糖皮质激素诱发的骨质疏松大鼠骨生物力学及骨密度的改善作用及其机制。方法:将3月龄的雌性Wister大鼠随机分为5组,即正常对照组、模型组(激素组)和人参皂苷高、中、低剂量组(激素+用药组)。皮下注射甲泼尼龙5mg/Kg.d-1,建立骨质疏松症模型。人参皂苷组造模后GSS高(100mg/kg)、中(50mg/kg)、低(25mg/kg),每日2次,其他2组给予等量生理盐水,实验期为9w。9w后测定各组大鼠骨密度(BMD)、骨代谢生化指标及骨生物力学指标等。结果:反映骨形成指标BGP、CT及血清Ca水平,模型组显著低于正常组,人参皂苷高剂量组显著高于模型组(P<0.05),反映骨吸收的TRACP酶活性及血清P水平,各组之间无统计学意义(P>0.05);与正常组比较,模型组大鼠腰椎与股骨骨密度、最大载荷及刚度均显著降低(P<0.05),且腰椎骨密度下降更为明显,与模型组比较,人参皂苷高剂量组大鼠腰椎及股骨骨密度、最大载荷及刚度均显著增高(P<0.05)。结论:人参皂苷GSS可通过改善骨代谢生化指标及骨生物力学性能,拮抗糖皮质激素性骨质疏松大鼠的骨丢失,起到防治骨质疏松的作用。

Objective：To investigate modifying impact and mechanism of Ginsenoside saponins （GSS） on bone biomechanics and bone density in glucocorticoid induced osteoporosis rats. Methods：Three month aged female Wister rats were randomly divided into 5 groups, namely the normal control group, model group （hormone treated ） and ginseng saponin in high, low, group plus hormone treatment. Subcutaneous injection of methylprednisolone （5 mg/Kg） to establish the osteoporosis model. Ginseng saponins groups were given GSS at respective dosages, i.e. high （100mg/kg） , medium （50 mg / kg ） , low （ 25 mg / kg ） , twice a day. The other two groups weregiven the same amount of normal saline. After 9W, rats＇bone mineral density （BMD） and biochemical markers of bone metabolism and bone biomcchanics were observed. Results ： The index of BGP, CT and Ca of the model group were significantly lower than those of the normal group, and of the high dosage GSS group （ P 〈 0. 05 ）. The difference of RACP and serum P were not signifiean~ among groups （ P 〉 0.05 ） ; Compared with normal group, the rats in the model group showed reduced lumbar and femoral bone mineral density, maximum load and stiffness （ P 〈 0. 05 ） , and a lumbar bone density decreased more significantly. Compared with the model group, those parame- ters were significantly higher in high dose group of ginsenosides rats （ P 〈 0.05 ）. Conclusion： Ginsenoside can prevent and treat osteopo- rosis by improving biochemical markers of bone metabolism and bone biomechanics and antagonizing bone loss in glucocorticoid reduce osteoporosis.