首页|减味寿胎丸介导PI3K/AKT/mTOR信号通路对米非司酮诱导HTR-8/SVneo细胞损伤模型血管生成功能的影响

减味寿胎丸介导PI3K/AKT/mTOR信号通路对米非司酮诱导HTR-8/SVneo细胞损伤模型血管生成功能的影响

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目的:探讨减味寿胎丸通过调控PI3K/AKT/mTOR信号通路对米非司酮诱导HTR-8/SVneo细胞损伤模型血管生成功能的影响.方法:收集自然流产患者以及正常妊娠女性绒毛组织各20例.构建米非司酮诱导HTR-8/SVneo细胞损伤模型,分为阴性对照组、模型组、孕酮组和减味寿胎丸组.采用CCK8法检测米非司酮对HTR-8/SVneo细胞以及减味寿胎丸对米非司酮诱导HTR-8/SVneo细胞损伤模型细胞增殖活力的影响.Western Blot测定血管内皮生长因子A(VEGFA)、血管内皮生长因子受体(VEGFR)1、VEGFR2以及信号通路PI3K、p-AKT、p-mTOR蛋白的表达.结果:与正常妊娠女性比较,自然流产患者绒毛组织VEGFA、VEGFR1、VEGFR2以及PI3K、p-AKT、p-mTOR信号通路蛋白的表达显著下调(P＜0.05,P＜0.01);不同浓度减味寿胎丸作用24 h均能显著增加米非司酮诱导HTR-8/SVneo细胞损伤模型的细胞活性(P＜0.05,P＜0.01);米非司酮诱导HTR-8/SVneo细胞损伤模型血管生成功能相关蛋白VEGFA、VEGFR1与VEGFR2蛋白表达显著下调(P＜0.01,P＜0.05),PI3K信号通路蛋白表达显著下降(P＜0.01),而减味寿胎丸能提高上述模型血管生成功能相关蛋白与PI3K/AKT/mTOR信号通路蛋白表达(P＜0.01,P＜0.05).结论:减味寿胎丸可能通过介导PI3K/AKT/mTOR信号通路提高米非司酮诱导HTR-8/SVneo细胞损伤模型VEGFA及其受体表达,从而起到补肾安胎作用.
Effects of Jianwei Shoutai Pills-mediated PI3K/AKT/mTOR signaling pathway on angiogenic function in Mifepristone induced HTR-8/SVneo cell injury model
Objective:To investigate the effects of Jianwei Shoutai Pills in regulating PI3K/AKT/mTOR signaling pathway on the angiogenic function of Mifepristone induced HTR-8/SVneo cell injury model.Methods:Twenty chorionic villus tissues were collected from spontaneous abortion patients(SA)and normal pregnant females(NP)respectively.A Mifepristone-induced HTR8-SVneo cell injury model was constructed and divided into negative control group,model group,progesterone group,and Jianwei Shoutai Pills group.The effects of Mifepristone on the growth of HTR-8/SVneo cells and the effects of Jianwei Shoutai Pills on the growth of Mifepristone-induced HTR-8/SVneo cell injury models were detected by CCK8.The expression of vascular endothelial growth factor A(VEGFA),vascular endothelial growth factor receptor(VEGFR)1,VEGFR2,and the signaling pathway PI3K,p-AKT,and p-mTOR-related proteins were measured by Western Blot.Results:The expression of VEGFA,VEGFR 1,VEGFR2 and signaling pathway PI3K,p-AKT,p-mTOR related proteins were down-regulated in the chorionic villus tissues of spontaneous abortion patients compared to normal pregnant women(P＜0.05,P＜0.01);Different concentrations of Jianwei Shoutai Pills for 24 hours increased the activity of mifepristone induced HTR-8/SVneo cell injury model(P＜0.05,P＜0.01);VEGFA,VEGFR1 and VEGFR2 expression were downregulated in the Mifepristone induced HTR-8/SVneo cell injury model(P＜0.05,P＜0.01),and PI3K signaling pathway protein expression was decreased(P＜0.01),while Jianwei Shoutai Pills increased the model angiogenic function related protein and PI3K/AKT/mTOR signaling pathway protein expression(P＜0.01,P＜0.05).Conclusion:The Jianwei Shoutai Pills may increase the expression of VEGFA and its receptor in the Mifepristone-induced HTR-8/SVneo cell injury model through mediating the PI3K/AKT/mTOR signaling pathway,thus playing a role in tonifying the kidney and calming the fetus.

Jianwei Shoutai PillsMifepristoneTrophoblastAngiogenesisSpontaneous abortion

黄娴、曾丽华、谢宝珍、李经纬、郜洁、罗颂平

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广州中医药大学第一临床医学院,广州 510405

广州中医药大学第一附属医院,广州 510405

减味寿胎丸 米非司酮 滋养细胞 血管生成 自然流产

国家自然科学基金面上项目青年岐黄学者培养项目广东省重点领域研发计划"岭南中医药现代化"重点专项广州市基础研究计划市校(院)联合资助市重点实验室建设项目

82174424国中医药人教函[2022]256号2020B1111100003202201020383

2024

中华中医药杂志
中华中医药学会

中华中医药杂志

CSTPCD北大核心
影响因子：1.135
ISSN：1673-1727
年,卷(期)：2024.39(9)