A2AR活化在脑创伤后tau蛋白过度磷酸化中的作用和机制分析

摘要

目的 研究A2AR活化在脑创伤后tau蛋白过度磷酸化中的作用和机制.方法 选择无特定病原体级的SD大鼠、SH-SY5Y进行培养,大鼠原代海马神经元分别加CGS21680溶液和DMSO,SH-SY5Y的观察组分别加CGS21680溶液,及sb216763、H-89,或只加ZM241385,对照组加DMSO,对比各组tau蛋白过度磷酸化情况.结果 大鼠原代海马神经元tau蛋白磷酸化水平明显高于对照组,差异有统计学意义(P＜0.05);SH-SY5Y细胞中,观察1组tau蛋白磷酸化水平明显升高,与其他组相比,差异有统计学意义(P＜0.05);观察2组和3组tau蛋白磷酸化水平明显高于对照组,差异有统计学意义(P＜0.05);观察4组和5组tau蛋白磷酸化水平与对照组比较,差异无统计学意义.结论 脑创伤后A2AR活化能够激活激酶A和GSK-3β,从而导致tau蛋白过度磷酸化.%Objective To study the role and mechanism of A2AR activation in tau hyperphosphorylation after brain injury.Methods SD rats were cultured with no specific pathogen level.SH-SY5Y was cultured.The rats were treated with CGS21680 solution and DMSO and SH-SY5Y respectively.The CGS21680 solution and sb216763, H-89, or Only add ZM241385, the control group plus DMSO, compared with each group tau hyperphosphorylation.Results The phosphorylation level of tau protein in SH-SY5Y cells was significantly higher than that in the control group (P<0.05).The phosphorylation level of tau protein in the primary hippocampal neurons of rats was significantly higher than that of the control group (P<0.05).The levels of tau protein phosphorylation in group 2 and group 3 were significantly higher than those in control group (P<0.05).The expression of tau in group 4 and group 5 was statistically significant (P<0.05)There was no significant difference in phosphorylation level between the two groups.Conclusion A2AR activation can activate kinase A and GSK-3β after brain injury, leading to tau hyperphosphorylation.