Modified Qing’ e Pills exerts anti-osteoporosis effects and prevents bone loss by enhancing type H blood vessel formation

骨保护素 内分泌学 血管生成 血管内皮生长因子 内科学 骨吸收 血管紧张素II 骨质疏松症 兰克尔 医学 化学 受体 激活剂(遗传学) 血管内皮生长因子受体
作者
Junjie Lu,Desheng Hu,Chen Ma,Xiaojuan Xu,Lin Shen,Jianhui Rong,Jia Zhao,Bo Shuai
出处
期刊:Frontiers in Endocrinology [Frontiers Media]
卷期号:13: 998971-998971 被引量:11
标识
DOI:10.3389/fendo.2022.998971
摘要

Objective: To explore whether the modified Qing' e Pills (MQEP) exerts anti-osteoporotic effects and prevents bone loss by enhancing angiogenesis. Methods: Network pharmacology was used to assess whether MQEP has a pro-angiogenic capacity and to predict its potential targets. Human umbilical vein endothelial cells were treated with glucocorticoids and MQEP to assess cell viability. The expression of angiotensin II type 1 receptor, angiotensin II type 2 receptor, and angiotensin converting enzyme, which are associated with the activation of the renin-angiotensin-aldosterone system, and the expression of vascular endothelial growth factor and hypoxia-inducible factor 1 alpha, which are associated with the formation of type H blood vessels, were examined by western blot and RT-qPCR. Thereafter, the glucocorticoid-induced osteoporosis model was established and intervened with MQEP. Femur scanning was performed with micro-computed tomography; trabecular spacing, trabecular thickness, and trabecular number were observed and calculated; the expression of nuclear factor-kappa B ligand and osteoprotegerin was detected by ELISA, and the ratio was calculated to evaluate the degree of bone resorption. Finally, type H blood vessels that were highly coupled to osteogenic cells were identified by immunohistochemistry staining and flow cytometry. Results: experiments confirmed that MQEP could effectively promote the proliferation of vascular endothelial cells and alleviate glucocorticoids-induced activation of the renin-angiotensin-aldosterone system, thereby reducing vascular injury. Conclusion: MQEP exerts anti-osteoporosis effects and prevents bone loss by alleviating vascular injury caused by renin-angiotensin-aldosterone system activation and promoting type H blood vessel formation.
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