论文部分内容阅读
目的探讨CDDO-E6对左旋谷氨酸(L-谷氨酸)诱导的人源性神经母细胞瘤(SH-SY5Y)神经细胞损伤的保护作用及其分子机制。方法 SH-SY5Y神经细胞分为空白对照组(A组)、L-谷氨酸损伤组(B组)、CDDO-E6+L-谷氨酸组(C组)、CDDO-E6单独处理组(D组)。使用MTT法检测细胞存活率,光学显微镜下观察细胞形态,用二氯荧光黄二乙酸酯(DCFH-DA)试剂检测细胞内活性氧(ROS)水平,Western blot法测定细胞质中细胞色素C(Cyt C)和磷酸化细胞外调节蛋白激酶1/2(p-ERK1/2)蛋白水平。结果与A组比较,B组细胞内ROS、Cyt C蛋白和p-ERK1/2蛋白水平增加(P<0.01或P<0.05),细胞存活率降低(P<0.01),D组无明显变化(P>0.05)。与B组比较,C组细胞内ROS、Cyt C和p-ERK1/2蛋白水平下降(P<0.05),SH-SY5Y神经细胞存活率改善(P<0.01)。结论 CDDO-E6对L-谷氨酸诱导的SH-SY5Y神经细胞损伤具有保护作用;其机制可能是通过降低细胞内ROS水平,减少线粒体释放Cyt C和下调p-ERK1/2蛋白水平。
Objective To investigate the protective effect of CDDO-E6 on neuronal injury of human neuroblastoma (SH-SY5Y) induced by L-glutamate (L-glutamate) and its molecular mechanism. Methods SH-SY5Y neurons were divided into blank control group (group A), L-glutamic acid injury group (group B), CDDO-E6 + L-glutamate group (group C) and CDDO-E6 alone treatment group Group D). Cell viability was detected by MTT assay. Cell morphology was observed under a light microscope. Reactive oxygen species (ROS) levels were measured by DCFH-DA reagent. Cyt C ) And phosphorylated extracellular regulated protein kinase 1/2 (p-ERK1 / 2) protein levels. Results Compared with group A, the levels of ROS, Cyt C and p-ERK1 / 2 in group B were increased (P <0.01 or P <0.05), the cell survival rate was decreased P> 0.05). Compared with group B, the levels of ROS, Cyt C and p-ERK1 / 2 in group C were decreased (P <0.05), and the survival rate of SH-SY5Y neurons was improved (P <0.01). Conclusion CDDO-E6 can protect L-glutamic acid-induced SH-SY5Y neurons from damage. Its mechanism may be through decreasing intracellular ROS levels, decreasing the mitochondrial release of Cyt C and down-regulating the protein level of p-ERK1 / 2.