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作 者:宋红梅[1,2] 吴斌[1] 魏迎辰[2] 李楠[2] 王和鸣[2]
机构地区:[1]福建中医药大学附属第二人民医院,福州350003 [2]福建中医药大学
出 处:《中国中医骨伤科杂志》2013年第12期1-3,7,共4页Chinese Journal of Traditional Medical Traumatology & Orthopedics
基 金:国家自然科学基金(编号81173283);福建省教育厅课题(JA13156)
摘 要:目的:探讨温阳补肾方对兔激素性股骨头坏死血清OPG、RANK、RANKL表达的影响,进一步揭示温阳补肾方对激素性股骨头坏死的作用机制。方法:136只新西兰大白兔随机分为正常组、模型组、中药低、中、高剂量组。造模成功后,分别于给药后第4、8、12周取血清,用酶联免疫法检测OPG/RANK/RANKL含量。结果:第4周时,正常组、中药中、高剂量组RANK、RANKL明显低于模型组(P<0.01),而OPG明显高于模型组(P<0.01)。第8周时,正常组、中药低、中、高剂量组RANK、RANKL明显低于模型组(P<0.01),而OPG明显高于模型组(P<0.01)。第12周时正常组、中药低、中、高剂量组RANK、RANKL明显低于模型组(P<0.01),而OPG明显高于模型组(P<0.01)。结论:大剂量激素使用可上调RANK、RANKL的表达,下调OPG的表达,使骨过度吸收从而破坏骨质导致股骨头坏死。温阳补肾方可以提高OPG表达,降低RANK、RANKL的表达,抑制破骨细胞的活化,促进新骨的形成,是治疗激素性股骨头坏死的作用机制之一。Objective:To explore the effects of Wenyangbushen formula on serum OPG, RANK and RANKL in model rabbits with steroid-induced avascular necrosis of femoral head (SANFH), and to investigate the underlying mechanisms.Methods.. One hundred and thirty-six New Zealand white rabbits were randomly divided into normal control, model group, and Wenyangbushen formula groups with low, medium and high doses. SANFH models were established by injection of steroid. After modeling, Wenyangbushen formula groups were treated by formula with different doses. The levels of OPG,RANK, and RANKL in blood were analyzed by ELISA at the 4th, 8th and 12th week after treatment in each group. Results:At the 4th week, the blood levels of RANK and RANKL in normal control, medium and high-dose groups were all lower than model group while OPG higher than model group(all P〈0.01). At the 8th week, the levels of RANK and RANKL in blood of normal group and the three treatment groups were all lower than model group, and OPG higher than model group (all P〈0.01). At the 12th week, the similar results were found to the 8th week. Concision: A large dose of steroid can cause excessive absorption of bone and bone destruction which will lead to femur head necrosis by up-regulating the expression of RANK and RANKL in blood and down-regulating the expression of OPG in blood. Wenyangbushen Formula can inhibit activation of osteoclast, thereby promote the formation of new bone by up-regulating the expression of OPG in blood and down-regulating the expression of RANK and RANKL in blood, which may be one of the underlying mechanisms.
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