Liuwei Dihuang Pill () 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
Liuwei Dihuang Pill () 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
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DOI：
10.1007/s11655-016-2744-2
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发表时间：
2018-06-01
影响因子：
2.9
通讯作者：
Ni, Chen-bo
中科院分区：
文献类型：
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作者：
Ge, Ji-rong;Xie, Li-hua;Ni, Chen-bo
为探讨六味地黄丸治疗肾阴虚型绝经后骨质疏松症（PMOP）的作用机制，将205例PMOP患者分为肾阴虚组（A组）、肾阳虚组（B组）、非肾虚组（C组）和对照组（N组）。采用实时荧光定量聚合酶链反应（RT-PCR）和Western blot技术观察LDP对心肌营养素样细胞因子1（CLCF 1）、锚蛋白重复序列和含SOCS盒1（ASB 1）的影响，和前动力蛋白2（PROK 2）基因以及Janus激酶/信号转导子和转录激活子A组CLCF 1基因mRNA（P < 0.05）和蛋白（P < 0.01）表达水平均显著低于N组相应水平。LDP治疗3个月后，CLCF 1基因mRNA表达水平明显上调（P < 0.01）。治疗6个月后，CLCF 1 mRNA和蛋白表达水平显著上调（均P < 0.01），股骨上端平均骨密度显著增加（P < 0.05）。CLCF 1基因是PMOP肾阴虚证的重要相关基因，LDP可能通过上调CLCF 1基因表达，激活JAK/STAT信号通路，从而发挥治疗作用。
To investigate the mechanism of Liuwei Dihuang Pill (, LDP) in treating postmenopausal osteoporosis (PMOP) with Shen (Kidney) yin deficiency.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 prokineticin 2 (PROK2) genes and the Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling pathway.The mRNA (P < 0.05) and protein (P < 0.01) expression levels of the CLCF1 gene 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 gene 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.The CLCF1 gene is an important gene associated with PMOP Shen-yin deficiency and the therapeutic effects of LDP may be mediated by up-regulation of CLCF1 gene expression and activation of the JAK/STAT signaling pathway.