Liuwei Dihuang Pill(六味地黄丸)Treats Postmenopausal Osteoporosis with Shen(Kidney) Yin Deficiency via Janus Kinase/Signal Transducer and Activator of Transcription Signal Pathway by Up-regulating Cardiotrophin-Like Cytokine Factor 1 Expression

作     者：GE Ji-rong XIE Li-hua CHEN Juan LI Sheng-qiang XU Hui-juan LAI Yu-lian QIU Long-long NI Chen-bo 

作者机构：Key Research Laboratory of Osteoporosis Syndrome Genomics Fujian Academy of Traditional Chinese Medicine Fuzhou 350003 China 

出 版 物：《Chinese Journal of Integrative Medicine》 (中国结合医学杂志（英文版）)

年 卷 期：2018年第24卷第6期

页      面：415-422页

核心收录：

学科分类：090603[农学-临床兽医学] 09[农学] 0906[农学-兽医学] 

基　　金：Supported by National Natural Science Foundation of China(Nos.81173280,81302995,81403420) Fujian Medical Innovation project(No.2011-CX-30) Science and Technology Department of Fujian Province autonomous non-profit research institutes topics project(No.2011R1038-5) Fujian Academy of Traditional Chinese autonomous topics Project(No.2012fjzyyk-5) 

主　　题：postmenopausal osteoporosis Chinese medicine Shen (Kidney) yin deficiency cardiotrophin- like cytokine factor 1 gone Liuwei Dihuang Pill Janus kinase/signal transducer and activator of transcription signaling pathway 

摘      要：Objectives： To investigate the mechanism of Liuwei Dihuang Pill （六味地黄丸, LDP） in treating postmenopausal osteoporosis （PMOP） with Shen （Kidney） yin deficiency. Methods： In this study, 205 cases of PMOP were divided into the PMOP Shen-yin deficiency group （Group A）, PMOP Shen-yang deficiency group （Group B）, PMOP without Shen deficiency group （Group C）, and control group （Group N）. Real-time polymerase chain reaction （RT-PCR） and Western blot techniques were used to observe the effects of LDP treatment on the cardiotrophin-like cytokine factor 1 （CLCF1）, ankyrin repeat and SOCS box containing 1 （ASB1）, and proldneticin 2 （PROK2） genes and the Janus kinase/signal transducer and activator of transcription （JAK/STAT） signaling pathway. Results： The mRNA （P〈0.05） and protein （P〈0.01） expression levels of the CLCF1 gone in Group A were significantly lower than the corresponding levels in Group N. After LDP treatment for 3 months, the mRNA expression levels of the CLCF1 gone were obviously up-regulated （P〈0.01）. After 6-month treatment, the expression levels of CLCF1 mRNA and protein were significantly up-regulated （both P〈0.01）, and the average bone density of the top femur had significantly increased （P〈0.05）. In vitro, CLCF1 overexpression resulted in a significant increase in the total protein and phosphorylated protein levels of JAK2 and STAT3. Conclusions： The CLCF1 gone is an important gone associated with PMOP Shen-yin deficiency and the therapeutic effects of LDP may be mediated by up-regulation of CLCF1 gone expression and activation of the JAK/STAT signaling pathway.