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The Aggravatory Effect of Nicotine on Ethanol-Induced
Acute Gastric Mucosa Injury: Role of Asymmetric
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Dimethylarginine#
LI Yuanjian, ZHANG Zhe, ZHOU Yuan, YANG Zhichun*
(Department of Pharmacology, School of Pharmaceutical Sciences, Central South University,
ChangSha 410078)
Abstract: effect of nicotine on ethanol-induced acute gastric injury. METHODS：Gastric mucosa
injury was induced by an injection of ethanol (75%) in the stomach in Sprague-Dawley rats. Animals
were pretreated with nicotine for 28 days. Nicotine was dissolved in tap water (0.05 mg/ml). The
gastric mucosal ulcer index (UI), the level of ADMA and NO were determined. Mucosal epithelium
cells were treated with nicotine (10 μM) for 24 h in the presence or absence of ethanol. The
concentrations of ADMA in the culture medium and the rate of cell apoptosis were determined.
RESULTS：In the rats treated with ethanol, the UI and ADMA level were increased and the NO level
was decreased, and the effects of ethanol were intensified by pretreatment with nicotine. Incubation of
nicotine (10 μM) with epithelial cells for 24 h further increased the elevated level of ADMA and rate of
cell apoptosis due to ethanol. Exogenous ADMA directly induced cell apoptosis. CONCLUSIONS：
The facilitatory effect of nicotine on ethanol-induced acute gastric mucosa injury is related to induction
of cell apoptosis by stimulation of ADMA generation.
Keywords: ADMA; apoptosis; ethanol; nicotine
1 Introduction
Nicotine, a major component of cigarette, has been proposed to be responsible for many
pharmacological effects of cigarette smoke. Epidemiological date showed that smoking not only
increased the incidence rate of acute gastric mucosa injury, but also provoked chronic peptic ulcer
[1, 2]. To what extent the gastric mucosa injury action is attributable to nicotine in cigarette smoke
remains poorly defined.
Gastric mucosa is composed of gastric endothelial cells and glands. Gastric endothelial cells
c
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