Modified Qing' e Pills exerts anti-osteoporosis effects and prevents bone loss by enhancing type H blood vessel formation.
Modified Qing' e Pills exerts anti-osteoporosis effects and prevents bone loss by enhancing type H blood vessel formation.
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改良的Qing'e药丸会施加抗po疏松症的作用，并通过增强H型血管形成来防止骨质流失。
DOI：
10.3389/fendo.2022.998971
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发表时间：
2022
影响因子：
5.2
通讯作者：
中科院分区：
文献类型：
--
作者：
探讨改良清鹅丸（MQEP）是否具有抗骨质疏松作用，并通过增强血管生成来防止骨质流失。使用网络药理学评估 MQEP 是否具有促血管生成能力并预测其潜在靶点。用糖皮质激素和 MQEP 处理人脐静脉内皮细胞以评估细胞活力。通过Western blot和RT-qPCR检测与肾素-血管紧张素-醛固酮系统激活相关的血管紧张素II 1型受体、血管紧张素II 2型受体和血管紧张素转换酶的表达，以及与H型血管形成相关的血管内皮生长因子和缺氧诱导因子1α的表达。此后建立糖皮质激素诱导的骨质疏松模型并采用MQEP进行干预。使用微型计算机断层扫描进行股骨扫描；观察并计算小梁间距、小梁厚度、小梁数量；采用ELISA法检测核因子-κB配体和骨保护素的表达，并计算比值来评价骨吸收程度。最后，通过免疫组织化学染色和流式细胞术鉴定出与成骨细胞高度偶联的H型血管。这是第一项研究揭示并证实MQEP可以通过促进与H型血管形成高度相关的缺氧诱导因子1α和血管内皮生长因子的表达来预防糖皮质激素引起的骨质疏松症中的骨丢失。体外实验证实，MQEP能有效促进血管内皮细胞增殖，减轻糖皮质激素引起的肾素-血管紧张素-醛固酮系统的激活，从而减轻血管损伤。 MQEP通过减轻肾素-血管紧张素-醛固酮系统激活引起的血管损伤，促进H型血管形成，发挥抗骨质疏松作用，防止骨质流失。
To explore whether the modified Qing’ e Pills (MQEP) exerts anti-osteoporotic effects and prevents bone loss by enhancing angiogenesis. 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. This is the first study to reveal and confirm that MQEP could prevent bone loss in glucocorticoid-induced osteoporosis by promoting the expression of hypoxia-inducible factor 1 alpha and vascular endothelial growth factor, which are highly associated with type H blood vessel formation. In vitro 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. 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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影响因子：
27.4
作者：
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通讯作者：
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