丙泊酚通过诱导自噬保护血管紧张素Ⅱ引起细胞损伤

Propofol protects angiotensin Ⅱ-induced cell injury by inducing autophagy

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.