Ethanol-induced oxidative stress is mediated by p38 MAPK pathway in mouse hippocampal cells.

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.

journal_name

Neurosci Lett

journal_title

Neuroscience letters

authors

Ku BM,Lee YK,Jeong JY,Mun J,Han JY,Roh GS,Kim HJ,Cho GJ,Choi WS,Yi GS,Kang SS

doi

10.1016/j.neulet.2007.03.049

subject

Has Abstract

pub_date

2007-05-23 00:00:00

pages

64-7

issue

1

eissn

0304-3940

issn

1872-7972

pii

S0304-3940(07)00373-4

journal_volume

419

pub_type

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