【摘要】 目的:研究黄芪甲苷（astragalosideⅣ,AS-Ⅳ）对缺氧损伤后人主动脉内皮细胞（human aortic endothelial cells,HAECs）的保护作用及对血管生成的影响及可能机制。方法:体外培养HAECs,8%O₂制备缺氧模型,实验分为对照组、缺氧组、AS-Ⅳ治疗组,50μg/mL)。观察AS-IV对缺氧损伤后HAECs的保护作用及对细胞迁移能力、增殖活性和体外成环的影响以及自噬在血管生成过程中的作用。结果:缺氧损伤后与对照组比较,HAECs细胞上清释放的损伤标志物乳酸脱氢酶（lactic dehydrogenase,LDH）浓度增加[（25.33±1.70）U/L vs.（5.33±1.25）U/L],细胞活力降低[（81.12±0.72）%vs.（100±3.07）%],细胞迁移能力降低,增殖能力降低,体外成环数下降[（30.91±3.78）个vs.（62.10±7.56）个],自噬相关蛋白Beclin及LC3-Ⅱ表达下调（P<0.05）。加入AS-Ⅳ治疗后,与缺氧组比较,细胞上清LDH释放量减少[（18.33±1.25）U/L],细胞活力提高[（85.71±2.48）%],细胞迁移能力增强、增殖活性增加,基质胶体外成环数增加[（48.64±4.80）个],自噬相关蛋白Beclin及LC3-Ⅱ表达上调（P<0.05）。结论:AS-Ⅳ可减轻缺氧对HAECs的损伤,可能通过激活自噬通路促进HAECs血管新生。更多还原

【Abstract】 Objective:The present study was designed to investigate the protection of astragaloside Ⅳ（AS-Ⅳ）on human aortic endothelial cells（HAECs）after hypoxia injury and underlying mechanism. Methods:HAECs were cultured in 8% O₂ to form hypoxic injury models. The cells were divided into control group（C）,hypoxic group（H）and AS-IV treatment group（AS-Ⅳ,50 μg/mL）. The protective effect of AS-Ⅳ on HAECs after hypoxia was observed,and the migration,proliferation and tube formation of the cells were analyzed. Autophagy related proteins were also identified. Results:Compared with the C group,the cells with hypoxia presented increased supernatant lactic dehydrogenase（LDH）concentration（25.33 ± 1.70 U/L vs. 5.33 ± 1.25 U/L）,decreased cell viability（81.12% ± 0.72% vs. 100.00% ± 3.07%）,cellular migration and proliferation ability and tube formation（30.91 ± 3.78 vs. 62.1 ±7.56）. Furthermore,the protein expression of Beclin and LC3-Ⅱ of the injured cells were decreased. After AS-Ⅳ treatment,compared with the H group,decreased LDH release（18.33 ± 1.25 U/L）,increased cell viability（85.71% ± 2.48%）,cellular migration and proliferation ability,and tube formation（48.64 ± 4.80）were observed. And the protein expression of Beclin and LC3-Ⅱ increased.Conclusion:AS-Ⅳ can alleviate hypoxia-induced damage and may promote angiogenesis of HAECs by the autophagy signaling pathway.更多还原