Abstract:
:Nicotine is one of the most representative components in cigarette smoke leading to gastric ulceration. Both ornithine decarboxylase and potassium ion (K(+)) channels are essential for cell growth and wound repair. The aim of the present study is to elucidate the causative relationship of these two factors during wound healing and the influence of nicotine on this healing process in rat gastric mucosal epithelial cells (RGM-1). Nicotine markedly inhibited cell migration and proliferation in RGM-1 cells. The latter effect was significantly antagonized by a nicotinic receptor blocker, mecamylamine. Nicotine also suppressed ornithine decarboxylase activity significantly. Our data showed that inhibition of cell proliferation and ornithine decarboxylase activity by nicotine was accompanied with a reduction in K(+) channel protein expression, all of which were significantly alleviated by spermidine pretreatment. These results suggested that there was a cause/effect link between ornithine decarboxylase and K(+) channel on wound repair. Nicotine in cigarette smoke inhibited this healing process and delayed wound repair in gastric epithelial cells.
journal_name
Eur J Pharmacoljournal_title
European journal of pharmacologyauthors
Shin VY,Liu ES,Koo MW,Luo JC,So WH,Cho CHdoi
10.1016/s0014-2999(02)01610-2keywords:
subject
Has Abstractpub_date
2002-05-24 00:00:00pages
115-21issue
1-2eissn
0014-2999issn
1879-0712pii
S0014299902016102journal_volume
444pub_type
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