丹黄散对高糖诱导血管内皮细胞AMPK/mTOR通路及自噬水平的影响OA
Effects of Danhuang Powder on AMPK/mTOR Pathway and Autophagy Level in Vascular Endothelial Cells Induced by High Glucose
目的 探讨丹黄散通过调控AMP 活化的蛋白质激酶(AMP-activated protein kinase,AMPK)/哺乳动物雷帕霉素靶蛋白(mammalian target of rapamycin,mTOR)通路和自噬水平对高糖诱导血管内皮细胞损伤的保护作用及其分子机制.方法 体外培养人脐静脉内皮细胞,设对照组(常规培养)、高糖组(30 mmol/L 葡萄糖)、高糖+生长因子组(30 mmol/L 葡萄糖+10%生长因子溶液)及高糖+丹黄散组(30 mmol/L 葡萄糖+10%丹黄散溶液),连续处理24 h.通过细胞划痕试验评估细胞迁移能力;采用免疫荧光法检测磷脂酰肌醇 3-激酶催化亚基 3 型(phosphatidylinositol 3-kinase catalytic subunit type 3,PIK3C3)基因和Beclin-1(BECN1)基因的表达水平;蛋白质印迹法(Western blot,WB)检测AMPK/mTOR通路关键蛋白及自噬标志物微管相关蛋白1 轻链3 α(microtubule-associated protein 1 light chain 3 alpha,LC3A)、微管相关蛋白 1 轻链 3β(microtubule-associated protein 1 light chain 3 beta,LC3B)的表达量.结果 丹黄散可促进高糖环境下的细胞迁移活性,增强PIK3C3 和Beclin-1 蛋白的表达,同时可上调AMPK及LC3A、LC3B蛋白的表达并下调mTOR蛋白表达.结论 丹黄散可通过激活AMPK/mTOR通路及上调自噬水平来减轻高糖诱导的血管内皮细胞损伤.
Objective To investigate the protective effect and molecular mechanism of Danhuang Powder a-gainst high glucose-induced vascular endothelial cells injury by regulating the AMPK/mTOR pathway and auto-phagy level.Methods An in vitro model of human umbilical vein endothelial cells was used and divided into a control group(normal culture),a high glucose group(30 mmol/L glucose),a high glucose+growth factor group(30 mmol/L glucose+10%growth factor solution),and a high glucose+Danhuang Powder group(30 mmol/L glucose+10%Danhuang Powder solution).All groups were treated continuously for 24 hours.Cell migration was assessed by wound healing assay.The expression levels of PIK3C3 and Beclin-1 were detected by immunofluorescence method.The expression of key proteins in the AMPK/mTOR pathway and autophagy mark-ers,including LC3A and LC3B,was determined by Western blot.Results Danhuang Powder enhanced cell migration activity under high glucose conditions,promoted the expression of PIK3C3 and Beclin-1 proteins,up-regulated the expression of AMPK,LC3A and LC3B proteins,and down-regulated the expression of mTOR protein.Conclusion Danhuang Powder alleviates high glucose-induced vascular endothelial cells injury by ac-tivating the AMPK/mTOR pathway and regulating autophagy level.
杨萱;赵月;张春玲;陈露;邸铁涛;高永跃;史青;赵思思;阎慧敏;向晋
贵州中医药大学,贵州 贵阳 550025贵阳市第一人民医院,贵州 贵阳 550002贵州中医药大学第二附属医院,贵州 贵阳 550003贵州中医药大学第二附属医院,贵州 贵阳 550003贵州中医药大学第二附属医院,贵州 贵阳 550003贵州中医药大学第二附属医院,贵州 贵阳 550003贵州中医药大学第二附属医院,贵州 贵阳 550003贵州中医药大学,贵州 贵阳 550025贵州中医药大学,贵州 贵阳 550025贵州中医药大学,贵州 贵阳 550025
医药卫生
丹黄散血管内皮细胞AMPK/mTOR信号通路自噬
Danhuang Powdervascular endothelial cellsAMPK/mTOR signaling pathwayautophagy
《贵州中医药大学学报》 2026 (2)
47-54,8
1.国家自然科学基金项目(81960805)2.2025年贵州省基础研究计划(自然科学)面上项目和重点项目(黔科合基础MS[2025]140)3.贵州省中医药管理局中医药、民族医药科学技术研究课题(QZYY-2025-011)4.贵州中医药大学研究生科研基金项目(YCXKYS2024009).
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