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目的研究MCI186对PC12细胞氧应激损伤的保护作用及其机制。方法以过氧化氢(H2O2)造成的PC12细胞氧应激损伤模型,采用MTT比色法、乳酸脱氢酶(LDH)活力测定,探讨了MCI186对PC12细胞氧应激损伤的影响;再用荧光染色技术及流式细胞仪测定在静息状态下的神经细胞内产生的过氧化氢含量。结果MCI186(1×10-6,1×10-5mol/L)可显著改善氧应激损伤引起的PC12细胞形态学变化,提高活细胞比率,对损伤的抑制率分别为407%及627%,并抑制细胞LDH释放;MCI186(1×10-7,1×10-6,1×10-5mol/L)还可降低静息状态下的神经细胞内过氧化氢的含量。结论MCI186可减少由H2O2诱导的细胞死亡,对PC12细胞氧应激损伤具有显著的保护作用;MCI186可能影响正常生理条件下细胞内过氧化氢的生成和/或神经细胞的氧化代谢过程,提示MCI186的自由基清除作用和抗氧化作用与其对脑缺血和脑缺血引起的脑水肿及组织损伤的保护作用密切相关。
Objective To investigate the protective effect and mechanism of MCI186 on oxygen stress injury in PC12 cells. Methods The oxidative damage of PC12 cells induced by hydrogen peroxide (H2O2) was examined by MTT colorimetric assay and lactate dehydrogenase (LDH) activity assay. The effects of MCI186 on oxygen stress injury in PC12 cells were investigated. Fluorescence Dyeing techniques and flow cytometry were used to measure the hydrogen peroxide content in resting nerve cells. Results MCI186 (1 × 10-6, 1 × 10-5mol / L) could significantly improve the morphological changes of PC12 cells induced by oxygen stress injury and increase the viable cell ratio, with the inhibition rates of 407% and 627%, respectively. And inhibited the release of LDH; MCI186 (1 × 10-7, 1 × 10-6, 1 × 10-5mol / L) could also reduce the content of hydrogen peroxide in resting nerve cells. Conclusion MCI186 can reduce cell death induced by H2O2 and protect PC12 cells against oxidative stress. MCI186 may affect the formation of intracellular hydrogen peroxide and / or oxidative metabolism of neurons under normal physiological conditions, suggesting that MCI186 Of free radical scavenging and anti-oxidant effects are closely related to their protective effect on brain edema and tissue damage caused by cerebral ischemia and cerebral ischemia.