摘要
目的探讨丙泊酚对血管紧张素II(Ang II)引起细胞损伤的保护机制。方法体外培养人脐静脉内皮细胞(HUVECs),建立AngⅡ损伤模型;实验分为正常对照组、AngⅡ组、AngⅡ+丙泊酚(AngⅡ+P)组、二甲基亚砜(DMSO)对照组、Ang 1-7抑制剂组。用CCK8检测细胞活性,免疫荧光染色检测细胞色素C,蛋白印迹法检测自噬相关蛋白LC3和P62表达。结果 AngⅡ最适宜作用浓度为10^(-6)mol/L,丙泊酚保护作用最适宜浓度为100μmol/L。AngⅡ组和DMSO组线粒体释放细胞色素C高于AngⅡ+P组(P<0.05),但其与Ang 1-7抑制剂组比较差异无统计学意义(P>0.05)。AngⅡ+P组P62表达水平略高于DMSO组,且自噬相关蛋白LC3-Ⅰ向LC3-Ⅱ转化亦增多,但差异均无统计学意义(P>0.05)。结论丙泊酚通过影响线粒体自噬途径抑制AngⅡ引起内皮细胞损伤。
Objective To study the protective mechanism of propofol on angiotensin Ⅱ (Ang Ⅱ )-induced cell injury. Methods Human umbilical vein endothelial cells (HUVECs) were used to establish the Ang Ⅱ -induced cell injury model, and divided into control (NC), Ang Ⅱ, Ang Ⅱ+propofol, dimethyl sulfoxide (DMSO) and Ang 1-7 inhibitor groups. Cell viability, and expression cytochrome C and autophagy related proteins LC3 and P62 were detected by CCK8, immunofluorescence, and Western blot, respectively. Results The most effect concentrations ofAng II and propofol were 10 6 mol/L and 100 μmol/L, respectively. The mitochondrial cytochrome C level was higher in AngII and DMSO groups than in Ang μ +propofol group (P〈0.05) but similar to that in Ang 1-7 inhibitor group (P〉0.05). P62 expression and conversion from LC3- I to LC3- Ⅱ were mildly upregulated in Ang Ⅱ +propofol group compared with DMSO group (P〉0.05). Conclusion Propofol can inhibit Ang Ⅱ -induced endothelial injury through autophagy pathway.
出处
《广东医科大学学报》
2017年第4期333-336,341,共5页
Journal of Guangdong Medical University
基金
国家自然科学基金(No.81270196
31301104
81470405)
广东医科大学附属医院博士启动项目(No.XB1343)