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目的观察丙酮酸对低氧诱导神经细胞损伤的保护作用及机制。方法采用丙酮酸处理PC12细胞,10 m L/L O2的低氧环境暴露12、24、48 h。MTT法观察细胞增殖情况,检测胱天蛋白酶3(caspase-3)活性观察细胞凋亡情况,ELISA检测白细胞介素1β(IL-1β)、IL-6、肿瘤坏死因子α(TNF-α)的水平,Western blot法检测p38丝裂原激活蛋白激酶(p38MAPK)、磷酸化的p38MAPK(p-p38MAPK)蛋白水平。结果低氧暴露24、48 h,抑制PC12细胞增殖,caspase-3活性增强,IL-1β、IL-6、TNF-α和p-p38MAPK水平增高;丙酮酸处理可显著增加PC12细胞增殖,减少细胞凋亡,降低IL-1β、IL-6、TNF-α水平,抑制p38MAPK的磷酸化水平。结论丙酮酸通过抑制p38MAPK的磷酸化而抑制低氧暴露引起PC12细胞炎症因子的表达,对低氧暴露导致的神经元损伤起保护作用。
Objective To observe the protective effect of pyruvate on hypoxic-induced neuronal injury and its mechanism. Methods PC12 cells were treated with pyruvate and exposed to 10, 20 and 24 h of hypoxia. The cell proliferation was observed by MTT assay. The apoptosis of caspase-3 was detected by enzyme-linked immunosorbent assay (ELISA). The levels of IL-1β, IL-6 and tumor necrosis factor α (TNF- The levels of p38 mitogen-activated protein kinase (p38MAPK) and phosphorylated p38MAPK (p-p38MAPK) protein were detected by Western blot. Results Exposure to hypoxia for 24 h and 48 h inhibited the proliferation of PC12 cells, increased the activity of caspase-3 and increased the levels of IL-1β, IL-6, TNF-α and p-p38MAPK. Pyruvate treatment significantly increased the proliferation of PC12 cells, Apoptosis and IL-1β, IL-6 and TNF-α levels were inhibited and phosphorylation of p38MAPK was inhibited. Conclusion Pyruvate inhibits the expression of inflammatory cytokines in PC12 cells induced by hypoxic exposure by inhibiting the phosphorylation of p38MAPK and protects the neurons from injury induced by hypoxia.