Date Published: November 20, 2011
Publisher: Hindawi Publishing Corporation
Author(s): Vivian Molina Cuevas, Yazmín Ravelo Calzado, Yohani Pérez Guerra, Ambar Oyarzábal Yera, Sonia Jiménez Despaigne, Rosa Mas Ferreiro, Daisy Carbajal Quintana.
Effects of GSE and vitamins C and E on aspirin- and ethanol-induced gastric ulcer and associated increases of lipid peroxidation in rats were compared. Two experiments were conducted. Rats were randomized into eight groups: a negative control and seven groups that received aspirin or ethanol for ulcer induction: one positive control (vehicle) and six with VC, VE, or GSE (25 and 250 mg/kg). Ulcer indexes and gastric levels of malondialdehyde (MDA) were quantified. VC, VE, and GSE (25 and 250 mg/kg) decreased aspirin, and ethanol-induced ulcers and MDA values compared with positive control group. The magnitude of aspirin ulcer reduction was comparable for all treatments, and MDA decrease with GSE was higher than with VC and tended to be greater, albeit none significantly, than with VE. GSE was more effective than VC and VE for lowering the ethanol ulcers, while the decrease of MDA levels with GSE was greater than with VC, but comparable to that achieved with VE. GSE protected against ethanol-induced gastric ulcers more effectively than VC or VE, while its protection against aspirin ulcers was comparable for all treatments. GSE produced the greatest reductions of gastric MDA in both models.
Peptic ulcer, a common gastrointestinal pathological condition, is due to the loss of the balance between aggressive and defensive factors of the gastric and duodenal mucosa. Aggressive factors against gastric mucosa include acid, pepsin, Helicobacter pylori, nonsteroidal anti-inflammatory drugs (NSAIDs), and ethanol, while local mucosal defensive factors include bicarbonate, mucus secretion, blood flow, cellular regeneration, and endogenous protective agents like prostaglandins (PG) and epidermal growth factors [1–3]. Also, increased oxidative stress is believed to be linked to the aggressive factors-induced gastric mucosal damage [4, 5].
Oral administration of GSE, VC, and VE, all at 25 and 250 mg/kg, prevented aspirin- and ethanol-induced gastric mucosal ulceration and reduced the increase of gastric MDA elicited by these aggressive agents. To our knowledge (Entrez PubMed review up to July 2011), this study is the first comparative study of the gastroprotective effect of GSE with those of VC and VE against aspirin- and ethanol-induced ulceration and concomitant increase of lipid peroxidation on the rat gastric mucosa.
GSE prevented ethanol-induced gastric ulcers more effectively than VC or VE, while its protection against aspirin ulcers was comparable for all treatments. GSE produced the greatest reductions of gastric MDA in both models. Then, the gastroprotective effects of GSE may be related, at least partially, to its ability for reducing lipid peroxidation in the gastric mucosa. Further studies must compare the therapeutic effects of GSE, VC, and VE on ethanol- and aspirin-induced gastric ulcer in rats.