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。
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.
出处
《中国临床药理学与治疗学》
CAS
CSCD
2005年第2期180-183,共4页
Chinese Journal of Clinical Pharmacology and Therapeutics