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作 者:贾乐生[1] 郑刚[1] 夏凡[1] 杨爽[1] JIA Lesheng ZHENG Gang XIA Fan YANG Shuang(Department of Orthopeadic Surgery, The Central Hospital Affiliated to Shenyang Medical College, Shenyang 110024, China)
机构地区:[1]沈阳医学院附属中心医院骨外三科,沈阳110024
出 处:《中国医科大学学报》2016年第12期1133-1135,1138,共4页Journal of China Medical University
摘 要:目的探讨氧化应激及抗氧化剂硫辛酸在大鼠骨质疏松发生中的作用及可能的机制。方法选用8周龄Wistar雌性大鼠24只,随机分为对照组、骨质疏松组和硫辛酸干预组,采用双侧卵巢切除法建立骨质疏松大鼠模型,硫辛酸组采用60 mg/kg硫辛酸腹腔注射,干预共8周;检测骨密度,全血碱性磷酸酶(ALP),骨钙素,钙、磷水平,股骨组织MDA、SOD和GSH-Px含量;Western blotting方法测定股骨组织护骨素(OPG)和细胞核因子κB受体活化因子配基(RANKL)蛋白含量,Real-time PCR方法测定股骨组织OPG和RANKL m RNA表达水平。结果骨质疏松组大鼠骨密度,股骨组织中SOD、GSH-Px、OPG m RNA及蛋白表达低于对照组大鼠(P<0.05);血清骨钙素,ALP水平,股骨组织中MDA、RANKL m RNA及蛋白水平都显著高于对照组大鼠(P<0.05)。硫辛酸组大鼠骨密度和股骨组织中SOD、GSH-Px、OPG m RNA及蛋白表达高于骨质疏松组大鼠(P<0.05);血清骨钙素,ALP水平,股骨组织中MDA、RANKL m RNA及蛋白表达水平都显著低于骨质疏松组大鼠(P<0.05)。结论氧化应激可能通过OPG/RANKL通路促进了大鼠骨质疏松的发生,而抗氧化剂硫辛酸可缓解骨质疏松的进展。Objective To investigate the effects of oxidative stress and lipoic acid (anfioxidant) on bone metabolism and explore the underlying mechanism. Methods A total of 24 Wistar rats aged 8 weeks were randomly divided into three groups. Osteoporosis rats model was established by bilateral ovaries deleted. Rat in lipoic acid group was injected with lipoic acid (60 mg/kg) for 8 weeks. The bone mineral density (BMD), steocalein, ALP, Ca, P, MDA, SOD and GSH-Px were detected. The levels of OPG and RANKL in serum were measured by Western blotting. OPG and RANKL mRNA were detected by real-time PCR. Results The level of BMD level in blood, SOD, GSH-Px, OPG mRNA and protein level in femur of osteoporosis group were significantly lower than the control group (P 〈 0.05 ). On the other hand, steocalcin, ALP, MDA, RANKL mRNA and protein level were significantly higher than the control group (P 〈 0.05 ). The level of BMD level in blood, SOD, GSH-Px, OPG mRNA and protein level of lipoic acid group were significantly higher than the osteoporosis group (P 〈 0.05 ). The steocalcin, ALP, MDA, RANKL mRNA and protein level were significantly lower than the osteoporosis group (P 〈 0.05). Conclusion Oxidative stress may increase osteoporosis through the upregulation of OPG / RANKL pathway in rats, and antioxidant lipoic acid can alleviate the progress of osteoporosis.
关 键 词:骨质疏松 硫辛酸 氧化应激 护骨素 细胞核因子κB受体活化因子配基
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