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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 To investigate the expression of granule protein precursor in L-glutamic acid induced SH-SY5Y cell oxidative stress injury model and its related mechanism. METHODS: SH-SY5Y cells were cultured and established L-glutamic acid induced oxidative stress injury model in SH-SY5Y cells. The expression of PGRN and its mechanism were detected by HE, IHC, WB and other related indicators. Results 1. The optimal concentration of L-glutamic acid to induce SH-SY5Y cell model was 12 mol / L and the best time was 24 h by CCK8 assay. In L-glutamate-induced cell model, The increase of glutamate concentration (0 mol / L, 6 mol / L, 12 mol / L) decreased the number of cells, increased the expression of PGRN, decreased the expression of ERK1 / 2 and the expression of Bax and Caspase- -2 expression gradually reduced, the results were statistically significant (P <0.05). Conclusions In SH-SY5Y cell model induced by L-glutamate, the number of cells gradually decreases and the expression of PGRN gradually increases with the increase of L-glutamic acid concentration. The mechanism may be through the regulation of ERK, Caspase and other signaling pathways .