Ethanol-induced oxidative stress is mediated by p38 MAPK pathway in mouse hippocampal cells
Ethanol-induced oxidative stress is mediated by p38 MAPK pathway in mouse hippocampal cells
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DOI：
10.1016/j.neulet.2007.03.049
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发表时间：
2007-05-23
影响因子：
2.5
通讯作者：
Kang, Sang Soo
中科院分区：
文献类型：
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作者：
Ku, Bo Mi;Lee, Yeon Kyung;Kang, Sang Soo
众所周知，乙醇通过氧化应激导致神经元细胞死亡。乙醇本身和由乙醇产生的活性氧（ROS）调节细胞内信号通路，包括丝裂原活化蛋白激酶（MAPK）级联反应。本研究旨在研究乙醇对HT22细胞中MAPK信号传导的影响。乙醇（100和400 mM）可激活ERK、p38 MAPK和JNK。ERK激活发生在早期，当ERK激活减弱时，p38 MAPK激活明显。p38 MAPK特异性抑制剂（SB203580）保护HT22细胞免受乙醇的侵害，同时抑制ROS的积累。然而，ERK （U0126）和JNK （SP600125）抑制剂在乙醇处理24小时后对乙醇诱导的神经元细胞死亡没有影响。这些结果表明，p38 MAPK可能在乙醇诱导的HT22细胞氧化应激过程中ROS积累中起重要作用。2007爱思唯尔爱尔兰有限公司版权所有。
It has been known that ethanol causes neuronal cell death through oxidative stress. Ethanol itself and reactive oxygen species (ROS) produced by ethanol modulate intracellular signaling pathways including mitogen-activated protein kinase (MAPK) cascades. This study was conducted to examine the impact of ethanol on MAPK signaling in HT22 cells. Ethanol (100 and 400 mM) caused activation of ERK, p38 MAPK, and JNK. ERK activation occurred in early time and p38 MAPK activation was evident when ERK activation was diminished. Specific inhibitor of p38 MAPK (SB203580) protected HT22 cells against ethanol, which was accompanied by an inhibition of ROS accumulation. However, inhibitors of ERK (U0126) and JNK (SP600125) had no effects on ethanol-induced neuronal cell death when they are treated with ethanol for 24 h. These results suggest that p38 MAPK may have important roles in ROS accumulation during ethanol-induced oxidative stress in HT22 cells. (c) 2007 Elsevier Ireland Ltd. All rights reserved.