首页|黄芪甲苷与丹参酮IIA配伍拮抗内皮细胞糖氧剥夺损伤促进血管新生

黄芪甲苷与丹参酮IIA配伍拮抗内皮细胞糖氧剥夺损伤促进血管新生

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目的 观察益气活血药对黄芪、丹参的有效活性成分黄芪甲苷(Astragaloside Ⅳ,AS-Ⅳ)与丹参酮ⅡA(Tanshinone ⅡA,Tan ⅡA)配伍拮抗内皮细胞糖氧剥夺(Oxygen-glucose deprivation,OGD)损伤的效应,探索其促进血管新生的作用及机制。方法 通过体外培养内皮细胞建立OGD损伤模型,实验设置对照组、模型组、AS-Ⅳ组、Tan ⅡA组和配伍组。分别采用CCK-8法、Transwell、体外血管形成实验观察AS-Ⅳ与Tan ⅡA配伍对内皮细胞增殖、迁移、成管能力的影响;利用AnnexinV-FITC细胞凋亡检测试剂盒检测内皮细胞的凋亡情况;免疫印迹法检测VE-cadherin、TGF-β1、VEGFA、eNOS的蛋白表达;免疫荧光法检测CD31、eNOS的蛋白表达;同时采用酶联免疫吸附法检测细胞培养上清液中一氧化氮(Nitric oxide,NO)的浓度。结果 与正常对照组相比,糖氧剥夺使HUVECs增殖、迁移与成管功能受损,诱导细胞凋亡,降低VE-cadherin、TGF-β1、VEGFA、CD31、eNOS的蛋白表达以及NO含量(P<0。01)。药物配伍组与模型组相比能修复损伤的内皮细胞,促进其增殖、迁移和成管,抑制糖氧剥夺诱导的细胞凋亡,提高VE-cadherin、TGF-β1、VEGFA、CD31、eNOS的蛋白表达以及NO含量(P<0。05)。结论 AS-Ⅳ与Tan ⅡA配伍具有拮抗内皮细胞糖氧剥夺损伤、激活血管新生反应的作用,其机制可能是激活eNOS,促进内皮细胞NO的生成与释放。
Combination of Astragaloside Ⅳ and Tanshinone Ⅱa Promote Angiogenesis after Oxygen-Glucose Deprivation Injury in Endothelial Cells
Objective The present study was designed to investigate the protection of Astragaloside Ⅳ(AS-Ⅳ)and Tanshinone Ⅱa(Tan Ⅱa)on human umbilical vein endothelial cells(HUVECs)after oxygen-glucose deprivation(OGD)injury and underlying mechanism.Methods HUVECs were cultured in vitro to establish the OGD injury model.The cells were divided into control group,model group,AS-Ⅳ group,Tan ⅡA group,and AS-Ⅳ+Tan ⅡA treatment group.The protective effect of AS-Ⅳ and Tan ⅡA combination on HUVECs after oxygen-glucose deprivation injury was observed,and the proliferation,migration,and tube formation of endothelial cells were analyzed.Apoptosis of HUVECs was determined using an AnnexinV-FITC apoptosis detection kit.The protein expressions of VE-cadherin,TGF-β1,VEGFA and Enos were detected by Western blotting.The expression of the proteins CD31 and Enos were detected by immunofluorescence.The concentration of nitric oxide(NO)in cell culture supernatants was also measured by ELISA.Results Compared with the control group,oxygen-glucose deprivation induced HUVECs dysfunction and apoptosis,and decreased the protein expression levels of VE-cadherin,TGF-β1,VEGFA,CD31,Enos as well as NO content(P<0.01).Compared with the model group,treatment group improved proliferation,migration and tube formation abilities of HUVECs,inhibited apoptosis,and increased the protein expression levels of VE-cadherin,TGF-β1,VEGFA,CD31,Enos as well as NO content(P<0.05).Conclusion AS-Ⅳ and Tan ⅡA can alleviate OGD-induced damage and may promote angiogenesis of HUVECs via upregulating the expression of Enos and enhancing the release of NO.

Oxygen-glucose deprivation injuryAstragaloside ⅣTanshinone ⅡaAngiogenesisEndothelial cellsEnosNO

张蕾、蔺琳、武继彪、李超

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山东中医药大学中医学院 济南 250355

山东中医药大学中医药创新研究院 济南 250355

糖氧剥夺损伤 黄芪甲苷 丹参酮ⅡA 血管新生 内皮细胞 内皮型一氧化氮合酶 一氧化氮

国家自然科学基金委员会青年基金项目山东省青年科技人才托举工程

SDAST2021qt08

2024

世界科学技术-中医药现代化
中科院科技政策与管理科学研究所,中国高技术产业发展促进会

世界科学技术-中医药现代化

CSTPCD北大核心
影响因子:1.175
ISSN:1674-3849
年,卷(期):2024.26(5)
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