Autophagy suppression by exercise pretreatment and p38 inhibition is neuroprotective in cerebral ischemia
Autophagy suppression by exercise pretreatment and p38 inhibition is neuroprotective in cerebral ischemia
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DOI：
10.1016/j.brainres.2014.08.067
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发表时间：
2014-10
期刊：
影响因子：
2.9
通讯作者：
Li Zhang;Wenxiu Niu;Zhijie He;Qi Zhang;Yi Wu;Congyu Jiang;Chaozheng Tang;Yongshan Hu;Jie Jia-J
中科院分区：
文献类型：
--
作者：
Li Zhang;Wenxiu Niu;Zhijie He;Qi Zhang;Yi Wu;Congyu Jiang;Chaozheng Tang;Yongshan Hu;Jie Jia-J
自噬是细胞蛋白质和细胞器的降解机制，但其在神经系统中的作用尚不清楚。本研究发现，运动预处理和抑制p38对脑缺血后的自噬过程有影响，这可能与运动预处理和抑制p38对脑缺血后自噬过程的影响有关。我们检测了脑缺血损伤后p62和磷酸化ERK 1/2的水平，分别作为自噬标志物和细胞存活标志物。测量缺血后脑梗死体积。跑台训练预处理和抑制p38均能降低p62的降解，促进ERK 1/2的磷酸化，减轻脑梗死，提示这些治疗方法可能通过抑制自噬对脑缺血损伤起到神经保护作用。
Autophagy is a degradative mechanism for cellular proteins and organelles, but its role in the nervous system is still not clear. In the present study, we found that exercise pretreatment and p38 inhibition had influence on autophagic process after cerebral ischemia, contributing to their neuroprotective effects. We examined the levels of p62 and phosphorylated ERK1/2 as an autophagic marker and cell-survival marker respectively after cerebral ischemic injury. The brain infarction volume after ischemia was measured as well. Both treadmill training pretreatment and p38 inhibition decreased the degradation of p62, promoted the phosphorylation of ERK1/2, and alleviated the brain infarction, indicating that these treatments could provide neuroprotection in cerebral ischemic injury via autophagy suppression.