柚皮素对氧化应激所致大鼠骨质疏松的影响及机制

Effect and Mechanism of Naringin on Osteoporosis Induced by Oxidative Stress in Rats

本研究为探究柚皮素对氧化应激所致大鼠骨质疏松的影响及机制。随机将60只SD大鼠分为正常组、模型组(醋酸泼尼松,5 mg/kg,12 w)和柚皮素治疗组(140 mg/kg,12 w),每组20只。柚皮素干预后,采用双能X线骨密度仪测定骨密度;采用ELISA法检测各组大鼠血清氧化应激相关指标超氧化物歧化酶(super oxide dismutase,SOD)、丙二醛(malondialdehyde,MDA)和护骨素(osteoprotegerin,OPG)含量;Western blotting检测磷脂酰肌醇-3-激酶(phosphatidylinositol-3-kinase,PI3K)的蛋白表达水平。模型组骨质疏松大鼠的腰椎和股骨骨密度、OPG含量和PI3K蛋白表达水平明显低于正常组大鼠(p<0.05);模型组骨质疏松大鼠的氧化应激水平明显高于正常组(p<0.05)。而模型组骨质疏松大鼠经抗柚皮素干预后,骨密度、OPG含量和PI3K蛋白表达水平明显升高,氧化应激水平明显降低。柚皮素可明显改善骨质疏松大鼠骨密度、OPG含量,其机制可能与降低氧化应激水平和改善PI3K通路有关。

In order to explore the effect and mechanism of naringin on osteoporosis induced by oxidative stress in rats.60 SD rats were randomly divided into normal group,model group(prednisone acetate,5 mg/kg,12 w),and naringin treatment group(140 mg/kg,12 w),20 rats in each group.After naringin intervention,bone mineral density was measured by dual energy X-ray absorptiometry;Superoxide dismutase(SOD),malondialdehyde(MDA)and osteoprotegerin(OPG)were measured by ELISA;Phosphatidylinositol-3-kinase was measured by Western blotting,PI3K.The BMD,OPG content and PI3K protein expression level of the model group were significantly lower than those of the normal group(p<0.05);The oxidative stress level of the model group was significantly higher than that of the normal group(p<0.05).In the model group,the bone mineral density,OPG content and PI3K protein expression level were significantly increased,while the oxidative stress level was significantly reduced.Naringin can significantly improve the bone mineral density and OPG content of osteoporosis rats,and its mechanism may be related to the reduction of oxidative stress level and the improvement of PI3K pathway.