Beihua University, Jilin City 132013, China.
Central Hospital, Jilin City 132013, China.
Biomed Res Int. 2019 Jul 4;2019:5962014. doi: 10.1155/2019/5962014. eCollection 2019.
Oxidative stress due to reactive oxygen species plays a central role in pathophysiology of neurodegenerative diseases. Inhibition of mitogen-activated protein kinase (MAPK) cascades attenuates the oxidative induced cell stress and behaves as potential neuroprotection agent.
In this study, we evaluate hydrogen peroxide induced neural cell stress and determine how different MAPK inhibitors restore the cell damage.
The results indicated that oxidative stress induced by neural cell damage commonly exists, and MAPK inhibitors partially and selectively attenuated the cell damage by reducing ROS production and cell apoptosis. The cultured neurons are more susceptible to hydrogen peroxide than subculture cells.
We conclude that the essential role of different MAPK inhibitors is to attenuate the hydrogen peroxide induced neuronal cell damage. Those data broaden the implication between individual neural cells and different MAPK inhibitors and give clues for oxidative stress induced neural diseases.
由于活性氧引起的氧化应激在神经退行性疾病的病理生理学中起着核心作用。丝裂原活化蛋白激酶（MAPK）级联的抑制可减轻氧化诱导的细胞应激，并表现出潜在的神经保护作用。
在这项研究中，我们评估了过氧化氢诱导的神经细胞应激，并确定了不同的 MAPK 抑制剂如何恢复细胞损伤。
结果表明，神经细胞损伤引起的氧化应激普遍存在，MAPK 抑制剂通过减少 ROS 产生和细胞凋亡，部分和选择性地减轻了细胞损伤。培养的神经元比亚培养细胞对过氧化氢更敏感。
我们得出结论，不同 MAPK 抑制剂的重要作用是减轻过氧化氢诱导的神经元细胞损伤。这些数据拓宽了个体神经元细胞和不同 MAPK 抑制剂之间的关系，并为氧化应激诱导的神经疾病提供了线索。
