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Clinical Trial Summary

For nearly 112 million patients with osteoporosis in China, it is of great significance for preventing and treating by clearly understanding the molecular mechanism of kidney deficiency. Thus, the research group has demonstrated in the earlier research that CLCF1 is an associated gene that can regulate JAK2/STAT3 signal pathway and impact bone metabolism for kidney yin deficiency of postmenopausal osteoporosis (PMOP). To make clear understanding of the direct-acting mechanism of CLCF1 for bone metabolism, this study intends to: ①observe impacts of low expression of CLCF1 upon immunities in mice and OPG/RANKL/RANK signal system using the technology of adenovirus associated virus. ②explore impacts of over-expression and silencing of CLCF1 on B lymphocytes by culcuturing the cells together with osteoblasts. ③ analyze the impacts of treating kidney yin deficiency of PMOP by Liuwei Dihuang pill upon immunities and OPG/RANKL/RANK system, and discuss the mechanism of regulating bone metabolism by CLCF1 by OPG/RANKL/RANK system via the bridge between immune system and bone metabolism, so as to demonstrate if the hypothesis of this study that "the molecular osteoimmunological mechanism of kidney yin deficiency of postmenopausal osteoporosis (PMOP) is possibly closely related to the impacts of CLCF1 regulation of OPG/RANKL/RANK signal system on bone metabolism" is right or not.


Clinical Trial Description

n/a


Study Design


Related Conditions & MeSH terms


NCT number NCT02981732
Study type Interventional
Source Fujian Academy of Traditional Chinese Medicine
Contact Yao xin
Phone 0591-83570813
Email yjyllbgs@163.com
Status Recruiting
Phase N/A
Start date October 2016
Completion date December 2020

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