丙泊酚通过MAPK/ERK信号通路对谷氨酸诱导的神经PC12细胞损伤的抑制作用

摘要

OBJECTIVE:To study inhibitory effects of propofol on PC12 cells injury induced by glutamic acid via mitogen-acti-vated protein kinase/extra-cellular regulated kinase (MAPK/ERK) signal pathway. METHODS:PC12 cells were randomized into normal control group,model group(10 mmol/L glutamic acid),propofol low-concentrations,medium-concentrations and high-con-centrations groups(12.5,25,50 μmol/L+10 mmol/L glutamic acid). The optical density of cells,cell apoptosis,the phosphoryla-tion of ERK1/2 and the expression of c-fos,Bax,Bcl-2 were detected after treated with relevant medicine for 48 h. RESULTS:Compared with normal control group,optical density of cells,the phosphorylation of ERK1/2 and Bcl-2 decreased in model group (P<0.01);apoptotic rate,the expression of c-fos and Bax increased (P<0.01). Compared with model group,optical density of cells,the expression of Bcl-2 and the phosphorylation of ERK1/2 increased in propofol group (P<0.01);apoptosis rate,the ex-pression of c-fos and Bax decreased (P<0.05 or P<0.01). There were statistical significant between the different concentrations (P<0.01). CONCLUSIONS:Propofol can inhibit the apoptosis of PC12 cells induced by glutamic acid,which is associated with the up-regulation of ERK1/2 phosphorylation.%目的:研究丙泊酚通过丝裂原激活的蛋白激酶/胞外信号调节的蛋白激酶(MAPK/ERK)信号通路对谷氨酸诱导的神经PC12细胞损伤的抑制作用.方法:取PC12细胞分为正常对照组、模型(10 mmol/L谷氨酸)组和丙泊酚低、中、高浓度(12.5、25、50μmol/L+10 mmol/L谷氨酸)组,分别加入相应药物,培养48 h后,检测各组细胞的光密度、凋亡情况和细胞中ERK1/2磷酸化水平及c-fos、Bax、B淋巴细胞瘤2(Bcl-2)的表达情况.结果:与正常对照组比较,模型组细胞的细胞光密度、磷酸化ERK1/2、Bcl-2表达均降低(P<0.01),凋亡率、c-fos和Bax表达均升高(P<0.01).与模型组比较,丙泊酚低、中、高浓度组细胞的光密度、磷酸化ERK1/2、Bcl-2表达均升高(P<0.01),凋亡率、c-fos和Bax表达均降低(P<0.05或P<0.01),且各浓度间差异有统计学意义(P<0.01).结论:丙泊酚可抑制谷氨酸诱导的PC12细胞凋亡,其可能与上调ERK1/2磷酸化水平有关.