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目的:研究丝裂原活化蛋白激酶信号通路抑制剂U0126对体外神经细胞缺氧损伤后细胞生长状态及水通道蛋白4(AQP4)表达的影响。方法:取出生1d的SD大鼠皮质神经细胞进行缺氧培养致细胞损伤,分为处理组和缺氧组,前者给予U0126,后者给予二甲基亚砜作为对照,检测AQP4的表达情况及细胞外信号调节蛋白激酶(ERK1/2)和Ets样因子(ELK1)蛋白磷酸化水平的变化。结果:缺氧损伤后细胞状态不佳,AQP4表达升高。给予U0126后ERK1/2和ELK1磷酸化水平降低,细胞状态有所改善,同时AQP4的表达降低。结论:缺氧损伤后细胞肿胀与AQP4的表达增高有关,U0126可抑制AQP4的表达,减轻细胞损伤。
AIM: To investigate the effect of U0126, a mitogen-activated protein kinase signaling pathway inhibitor, on cell growth status and AQP4 expression in vitro after hypoxic injury. Methods: Cortical neurons of SD rats were sacrificed and cultured for 1 hour. The cells were divided into treatment group and hypoxia group. The former was given U0126, and the latter was given dimethyl sulfoxide as control. The expression of AQP4 and Changes in phosphorylation of extracellular signal-regulated protein kinase (ERK1 / 2) and Ets-like factor (ELK1) proteins. Results: After hypoxia, the cell status was poor and AQP4 expression was increased. After U0126 administration, ERK1 / 2 and ELK1 phosphorylation levels were decreased, cell status was improved, and AQP4 expression was decreased. Conclusion: The cell swelling after hypoxia injury is related to the increase of AQP4 expression. U0126 can inhibit the expression of AQP4 and reduce the cell injury.