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 Lettjournal_title
Neuroscience lettersauthors
Ku BM,Lee YK,Jeong JY,Mun J,Han JY,Roh GS,Kim HJ,Cho GJ,Choi WS,Yi GS,Kang SSdoi
10.1016/j.neulet.2007.03.049subject
Has Abstractpub_date
2007-05-23 00:00:00pages
64-7issue
1eissn
0304-3940issn
1872-7972pii
S0304-3940(07)00373-4journal_volume
419pub_type
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