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[目的]探讨p38有丝分裂原活化蛋白激酶(p38MAPK)信号通路在大鼠睡眠剥夺中的作用及与炎症因子的关系。[方法]将40只雄性Wistar大鼠随机分为对照组、大平台组、小平台睡眠剥夺组、抑制剂组,每组10只。采用免疫组化观察大鼠海马区IL-1和磷酸化p38MAPK的表达,同时利用水迷宫检测大鼠认知功能。[结果]与对照组和大平台组对比,睡眠剥夺组IL-1β与磷酸化p38MAPK表达明显上调(P﹤0.05),抑制剂组显著下降(P﹤0.05)。认知功能评价中睡眠剥夺组明显低于对照组和大平台组(P﹤0.05),抑制剂治疗组明显改善(P﹤0.05)。[结论]p38MPAK信号转导通路参与了大鼠睡眠剥夺的过程,且可引起炎症因子的释放,该作用可影响大鼠认知功能。
[Objective] To investigate the role of p38 mitogen-activated protein kinase (p38MAPK) signaling pathway in sleep deprivation in rats and its relationship with inflammatory cytokines. [Methods] Forty male Wistar rats were randomly divided into control group, large platform group, small platform sleep deprivation group and inhibitor group, with 10 rats in each group. Immunohistochemistry was used to observe the expression of IL-1 and phospho-p38MAPK in hippocampus of rats. At the same time, the cognitive function of rats was detected by water maze. [Results] Compared with the control group and the large platform group, the expressions of IL-1β and phosphorylated p38MAPK in sleep deprivation group were significantly increased (P <0.05), while those in inhibitor group were significantly decreased (P <0.05). In the cognitive function evaluation, the sleep deprivation group was significantly lower than the control group and the large platform group (P <0.05), and the inhibitor treatment group was significantly improved (P <0.05). [Conclusion] The p38MPAK signal transduction pathway is involved in the process of sleep deprivation in rats and can cause the release of inflammatory cytokines, which may affect the cognitive function of rats.