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Abstract
Excessive ethanol ingestion causes gastric mucosal damage through the inflammatory
and oxidative processes. The present study was aimed to evaluate the protective effect
of thalidomide on ethanol-induced gastric mucosal damage in mice. The animals were
pretreated with vehicle or thalidomide (30 or 60 mg/kg, orally), and one hour later,
the gastric mucosal injury was induced by oral administration of acidified ethanol.
The animals were euthanized one hour after ethanol ingestion, and gastric tissues
were collected to biochemical analyzes. The gastric mucosal lesions were assessed
by macroscopic and histopathological examinations. The results showed that treatment
of mice with thalidomide prior to the administration of ethanol dose-dependently reduced
the gastric ulcer index. Thalidomide pretreatment significantly reduced the levels
of pro-inflammatory cytokines [tumor necrosis factor (TNF)-α, interleukin (IL)-1β,
IL-6], malondialdehyde (MDA) and myeloperoxidase (MPO) activity. In addition, thalidomide
significantly inhibited ethanol-induced nitric oxide (NO) overproduction in gastric
tissue. Histological observations showed that ethanol-induced gastric mucosal damage
was attenuated by thalidomide pretreatment. It seems that thalidomide as an anti-inflammatory
agent may have a protective effect against alcohol-induced mucosal damage by inhibition
of neutrophil infiltration and reducing the production of nitric oxide and inflammatory
cytokines in gastric tissue.