【摘要】 目的 :观察血管紧张素 (1 7) [Ang (1 7) ]对血管紧张素II(AngII)致人脐静脉内皮细胞 (HU VECs)损伤的保护作用。方法 :体外培养的HUVECs随机分为 4组 :对照组 ,AngII组 ,Ang (1 7)组 ,AngII+Ang (1 7)组。采用分光光度计测定培养的HU VECs乳酸脱氢酶 (LDH)漏出 ;流式细胞仪检测细胞凋亡 ;硝酸还原酶法和放射免疫分析技术分别测定HUVECs上清液中一氧化氮 (NO)和内皮素 1(ET 1)的含量。结果 :与对照组比较 ,AngII(0 .1μmol·L-1)显著增加HUVECsLDH漏出 (P <0 .0 1)、ET 1分泌(P <0 .0 1)和HUVECs凋亡率 (P <0 .0 1) ,显著减少NO的含量 (P <0 .0 5 ) ;Ang (1 7)呈剂量依赖性抑制了AngII的促LDH漏出、ET 1分泌、增加细胞凋亡等作用 ,同时明显促进HUVECs的NO释放 ;单用Ang (1 7)对HUVECs无明显影响。结论 :Ang (1 7)可抑制AngII所致的体外培养HUVECs损伤 ,对内皮细胞具有保护作用。更多还原

【Abstract】 AIM: To investigate the protective effects of angiotensin (1 7) [Ang (1 7)] on human umbilical vein endothelial cells (HUVECs) injury induced by angiotensin II (Ang II) in culture. METHODS: Cultured human umbilical vein endothelial cells were randomly divided into 4 groups: control, Ang II, Ang (1 7), and AngII+Ang (1 7). Spectrophotometer and flow cytometry were used to evaluate lactate dehydrogenase (LDH) leakage content and apoptosis percentage, respectively. Nitric oxide (NO) and endothelin 1 (ET 1) contents were measured by colorimetry and radioimmunoassay. RESULTS: 0.1 μmol·L -1 Ang II significantly increased LDH leakage (P< 0.01 ), ET 1 release (P< 0.01 ), and apoptosis percentage (P< 0.01 ). These increases were inhibited by Ang (1 7) in a dose dependent manner, while NO release by HUVECs was promoted by Ang (1 7). Ang (1 7) alone had no effect on HUVECs. CONCLUSION: Ang (1 7) has a protective effect on HUVECs via inhibition of Ang II induced injury and apoptosis, suggesting that Ang (1 7) may play an important role in prevention and treatment of vascular diseases.更多还原