Excessive alcohol consumption can lead to gastric ulcer and the present work was aimed to evaluate the potential beneficial effect of alpha lipoic acid (ALA) administration on ethanol induced gastric mucosa erosion in rats. This study was carried out on 60 male rats. The rats were divided into four equal groups of 15 rats each. Group Ι :( Control group): received no drugs. Group Π :( ulcerated non-treated group): administered with a single oral dose of 1 ml/rat of absolute ethanol for gastric ulcer induction. Group III :( ulcerated + ALA protected group): received alpha lipoic acid(100 mg/kg body weight/day) orally for 7 days before ethanol administration for the gastric erosion induction. Group IV :(ulcerated + ALA treated group) received alpha lipoic acid as in group III and the treatment was continued for 10 days later. Blood samples for serum separation were collected at the 8th. and 18th. days from the onset of treatment with ALA for the determination of serum nitric oxide (NO), sialic acid (SA), tumor necrosis factor-alpha (TNF-α), Interleukin-6 (IL-6) and L- Malondialdehyde (L-MDA). Also, gastric tissue specimens were collected for determination of (L-MDA), vitamin C, Glutathione peroxidase (GPx), Superoxide dismutase (SOD), Catalase (CAT),Glutathione reductase (GR), reduced glutathione (GSH), DNA-fragmentation and myeloperoxidase (MPO) activity. The results showed that ethanol induced gastric damage caused significant decreased in serum (NO) and (SA) concentrations and in gastric tissue vitamin C level, GPX, SOD, and CAT activities. On the other hand, a marked increase in TNF-α, IL-6, MPO, L-MDA, GR and DNA-fragmentation were observed in ethanol induced gastric damage. Pretreatment of ALA was able to mitigate gastric mucosa damage induced by ethanol through increasing of SA, vitamin C, SOD, CAT, GSH in addition to decreasing DNA-fragmentation and MPO in gastric tissue. The results of the present study suggest that, ALA may be effective in enhances the healing of gastric ulcers by its radical scavenging and antiapoptotic activity, adjusting the pro-inflammatory cytokine, inhibited neutrophil accumulation and regenerating endogenous antioxidant mechanisms.
Key Words
α-lipoic acid; Ethanol; Apoptosis; Pro-inflammatory Cytokines; Antioxidant enzymes.
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