从痰论治激性股骨头坏死OPGRANKRANKL信号调控机制研究进展.docVIP

从痰论治激性股骨头坏死OPGRANKRANKL信号调控机制研究进展.doc

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从痰论治激性股骨头坏死OPGRANKRANKL信号调控机制研究进展

从痰论治激素性股骨头坏死OPGRANKRANKL信号调控机制研究进展   摘要:近年来,激素的不规范使用导致激素性股骨头坏死(SANFH)的发病率呈上升趋势。中医药防治SANFH疗效确切,受到广泛关注,但由于缺乏药效学机理的分子生物学依据,尚未达到标准化治疗水平。OPG/RANK/RANKL信号通路的发现,为临床防治骨代谢疾病开辟了新途径。该信号通路与SANFH“脾虚生痰-由痰致瘀-因瘀致痹”的病机演变密切相关,从痰论治SANFH的分子生物学效应最终可通过该信号通路调控的微观信息来表达。本文探讨从痰论治SANFH与OPG/RANK/RANKL信号调控机制的相关性,结合骨代谢调控机制探讨SANFH的中医辨治,为临床及深入研究提供依据。 中国论文网 /1/viewhtm  关键词:激素性股骨头坏死;OPG/RANK/RANKL信号通路;从痰论治;机制;综述   DOI:10.3969/j.issn.1005-5304.2017.10.036   中图分类号:R272.968.1 文献标识码:A 文章编号:1005-5304(2017)10-0133-04   Research Progress in OPG/RANK/RANKL Signal-regulated Mechanism of Steroid Induced Avascular Necrosis of Femoral Head from Phlegm Theory WANG Xiao-min1, CAO Lin-zhong1, SONG Min1, LI Jun2, ZHAO Xi-yun1, LIU Xin-yu1, SU Liang-lei1 (1. Gansu University of Chinese Medicine, Lanzhou 730000, China; 2. Lanzhou University, Lanzhou 730000, China)   Abstract: In recent years, due to the irregular and abused use of glucocorticoid in clinical treatment, the incidence of steroid induced avascular necrosis of femoral head (SANFH) is gradually increasing. TCM for the prevention and treatment of SANFH has received much attention from many scholars. However, due to the lack of the scientific explanation of molecular biology level for its pharmacodynamics mechanism, it is difficult to achieve the purpose of standardized treatment. The discovery of OPG/RANK/RANKL signaling pathway has opened up new shortcuts for the prevention and treatment of bone metabolic diseases. OPG/RANK/RANKL signaling pathway is associated with the pathogenesis of “spleen deficiency and phlegm - blood stasis caused by phlegm-blood stasis due to paralysis” of SANFH. The treatment efficacy based on the phlegm theory can eventually axial control of the system through the micro-information to express. This article discussed the relevance between the “phlegm” in the treatment of SANFH and molecular biology mechanism of OPG/RANK/RANKL signal regulation mechanism, and combined the system of bone metabolism regulation mechanism to

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