颗粒蛋白前体在L-谷氨酸诱导SH-SY5Y细胞氧化应激损伤模型中的表达及作用机制

The expression and mechanism of PGRN in SH-SY5Y cells Oxidative Stress injury models induced by L-glutamic

目的探讨颗粒蛋白前体在L-谷氨酸诱导的SH-SY5Y细胞氧化应激损伤模型中表达及相关作用机制。方法培养SH-SY5Y细胞;建立L-谷氨酸诱导SH-SY5Y细胞氧化应激损伤模型;利用HE、免疫组化、WB等相关指标检测PGRN的表达及其作用机制。结果 1。通过CCK8法检测,L-谷氨酸诱导SH-SY5Y细胞模型的最佳作用浓度为12 mol/L,最佳作用时间为24 h;在L-谷氨酸诱导的细胞模型中,随着L谷氨酸浓度的增加(0 mol/L、6 mol/L、12 mol/L),细胞数量逐渐减少,PGRN表达逐渐增加,ERK1/2表达逐渐减少,Bax、Caspase-3表达逐渐增加,Bcl-2表达逐渐减少,结果具有统计学意义(P<0.05)。结论在L-谷氨酸诱导的SH-SY5Y细胞模型中,随着L-谷氨酸浓度增加,细胞数量逐渐减少,PGRN表达逐渐增多,其作用机制可能通过调控ERK、Caspase等信号通路来实现。

Objective This study aimed at exploring the expression and mechanism of PGRN in L-glutamic induce SHSY5 Y cells Oxidative Stress injury. Methods Cultured SH-SY5 Y cells. 2. Set up the SH-SY5 Y cells injury models induced by L-glutamic. Detecting the expressing of PGRN and searching for the mechanism of it in HE, immunohistochemistry and Western blot.Results The optimal concentration of the model was 120 mmol/L and the action time of it was 24 h by CCK-8. In the cell models,with the increase of L-glutamic concentration(0 mmol/L,50 mmol/L and 100 mmol/L),the number of cells reduce gradually,by the time,the expression of PGRN increased,the expression of ERK1/2 to reduce gradually,gradually increased the expression of Bax and Caspase 3,the Bcl- 2 expression gradually reduce. The result had a significant difference(P < 0.05). Conclusion In the SH-SY5 Y cells injury models induced by L-glutamic,as the increasing of L-glutamic concentration,the number of cells reduced gradually,however,the expression of PGRN increased. It may related to the signal pathway of ERK and Caspase。