TAK1对大鼠海马神经元细胞缺氧复氧后JNK信号通路和细胞凋亡的影响

发布时间：2019-05-23 13:02

【摘要】：目的探讨TAK1对大鼠海马神经元缺氧复氧后JNK信号通路和细胞凋亡的影响。方法新生(出生24 h)SD大鼠,雌雄不拘,体质量5~6 g,原代培养海马神经元,接种于培养孔或培养皿中。采用随机数字表法,将其随机分为4组,每组48孔和12皿,正常对照组(C组):不予任何处理;缺氧复氧组(HR组):缺氧4 h复氧24 h;TAK1抑制剂组(T组)、DMSO组:分别于缺氧处理前给予TAK1特异性抑制剂5Z-7-oxozeaenol 1μg/m L和等量DMSO溶液后行缺氧复氧。各组缺氧复氧处理结束后1 h,测定神经元活力、凋亡率、cleaved Caspase-3和Bax蛋白的表达水平,测定JNK磷酸化水平。结果与C组比较,HR组和DMSO组的海马神经元活力降低,细胞凋亡率升高,cleaved Caspase-3和Bax蛋白表达上调,JNK磷酸化水平明显升高(P0.05);与HR组比较,T组海马神经元活力增强,细胞凋亡率降低,cleaved Caspase-3和Bax蛋白表达下调,JNK磷酸化水平降低(P0.05)。结论 TAK1可能通过激活JNK信号通路介导的细胞凋亡参与大鼠海马神经元缺氧复氧后的损伤机制。
[Abstract]:Objective to investigate the effect of TAK1 on JNK signaling pathway and apoptosis in rat hippocampal neurons after hypoxia and reoxygenation. Methods Neonatal (24 h) SD rats), male and female, weighing 5 g or 6 g, primary cultured hippocampal neurons were inoculated in culture foramen or petri dish. The patients were randomly divided into 4 groups with 48 holes and 12 dishes in each group, normal control group (group C) without any treatment, anoxic reoxygenation group (HR group) for 24 hours, hypoxia group (group C), hypoxia group (group C) and hypoxia group (group C). TAK1 inhibitor group (T group), DMSO group: TAK1 specific inhibitor 5Z-7-oxozeaenol 1 渭 g / mL and the same amount of DMSO solution were given respectively before hypoxia treatment). The neuronal activity, apoptosis rate, the expression of cleaved Caspase-3 and Bax protein and the phosphorylation of JNK were measured at 1 h after hypoxia and reoxygenation treatment. Results compared with group C, the activity of hippocampal neurons in HR group and DMSO group was decreased, the apoptosis rate was increased, the expression of cleaved Caspase-3 and Bax protein was up-regulated, and the phosphorylation level of JNK was significantly increased (P 0.05). Compared with HR group, the activity of hippocampal neurons in T group was increased, the apoptosis rate was decreased, the expression of cleaved Caspase-3 and Bax protein was down-regulated, and the phosphorylation level of JNK was decreased (P 0.05). Conclusion TAK1 may be involved in the injury mechanism of rat hippocampal neurons after hypoxia and reoxygenation by activating JNK signaling pathway mediated apoptosis.
【作者单位】：广东三九脑科医院麻醉科;广东省中山市人民医院麻醉科;广东省佛山市第一人民医院麻醉科;
【分类号】：R614

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