| Literature DB >> 17420100 |
Bo Mi Ku1, Yeon Kyung Lee, Joo Yeon Jeong, Jihye Mun, Jae Yoon Han, Gu Seob Roh, Hyun Joon Kim, Gyeong Jae Cho, Wan Sung Choi, Gwan-su Yi, Sang Soo Kang.
Abstract
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 400mM) 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 24h. These results suggest that p38 MAPK may have important roles in ROS accumulation during ethanol-induced oxidative stress in HT22 cells.Entities:
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Year: 2007 PMID： 17420100 DOI： 10.1016/j.neulet.2007.03.049
Source DB: PubMed Journal: Neurosci Lett ISSN： 0304-3940 Impact factor: 3.046