Abstract
BackgroundBael (Aegle marmelos (L.) Corr.) has been widely used in indigenous systems of Indian medicine to exploit its medicinal properties including astringent, antidiarrheal, antidysenteric, demulcent, antipyretic, antiulcer, anti-inflammatory and anti cancer activities. The present study aims to evaluate the antioxidative and antiulcer effect of methanolic extract of unripe fruit of Aegle marmelos (MEAM) against Helicobacter pylori-Lipopolysaccharide (HP-LPS) induced gastric ulcer in Sprague Dawley (SD) rats.MethodsDose and duration of HP-LPS and MEAM were fixed based on ulcer index of gastric tissue of experimental animals. Various gastric secretory parameters such as volume of gastric juice, free and total acidity, acid output, pepsin concentration were analyzed. The activities of enzymatic antioxidants (superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and glutathione transferase), non-enzymatic antioxidants (reduced glutathione, vitamin C and vitamin E) and the levels of lipid peroxidation products were measured. Histological analysis was performed to evaluate the effect of Aegle marmelos on HP-LPS induced gastric ulcer.ResultsOral administration of HP-LPS (50 μg per animal) for four consecutive days resulted in induction of ulcer with the increase in gastric secretory parameters such as volume of gastric juice, free and total acidity, acid output, pepsin concentration. Oral administration of methanolic extract of Aegle marmelos fruit (MEAM) (25, 50, 100, 250 and 500 mg/kg) reduced the gastric ulcer by 2.8 %, 52.4 %, 73 %, 93 % and 93.98 %, respectively, compared to 89.2 % reduction by sucralfate (100 mg/kg). MEAM treatment significantly (p < 0.05) inhibited the increase in gastric secretory parameters in ulcerated rats, and it also prevented the reduction of enzymatic (superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and glutathione transferase) and non-enzymatic antioxidants (reduced glutathione, vitamin C and vitamin E) after HP-LPS induction. In addition, lipid peroxidation was inhibited by MEAM in HP-LPS induced rats. Results of histological analysis correlated well with biochemical parameters.ConclusionThese observations explored the antioxidant properties of MEAM contributing to the gastroprotective effect in HP-LPS induced gastric ulcer model.
Highlights
Bael (Aegle marmelos (L.) Corr.) has been widely used in indigenous systems of Indian medicine to exploit its medicinal properties including astringent, antidiarrheal, antidysenteric, demulcent, antipyretic, antiulcer, anti-inflammatory and anti cancer activities
The gastric mucosal responses associated with H. pylori infection in humans as well as those characterizing mucosal inflammatory changes in the animal model of Helicobacter pylori-Lipopolysaccharide (HP-LPS) induced gastritis are manifested by a marked increase in epithelial cell apoptosis and proinflammatory interleukin expression, excessive nitric oxide and prostaglandin generation, and the disturbances in NFκB and MAPK signaling cascades [15,16,17,18]
HP-LPS has been implicated in the stimulation of pepsinogen and histamine secretion, inhibition of sulfated mucin synthesis, and the production of potentially destructive auto-antibodies, which may all contribute to the loss of mucosal integrity [19]
Summary
Bael (Aegle marmelos (L.) Corr.) has been widely used in indigenous systems of Indian medicine to exploit its medicinal properties including astringent, antidiarrheal, antidysenteric, demulcent, antipyretic, antiulcer, anti-inflammatory and anti cancer activities. Helicobacter pylori, being a Gram-negative bacterium that colonizes the gastric mucosa, is recognized as a primary cause of gastric disease, and its cell-wall lipopolysaccharide has been identified among the key virulence factors responsible for eliciting mucosal inflammatory responses that characterize gastritis and duodenal ulcers [10,11,12,13,14]. The gastric mucosal responses associated with H. pylori infection in humans as well as those characterizing mucosal inflammatory changes in the animal model of HP-LPS induced gastritis are manifested by a marked increase in epithelial cell apoptosis and proinflammatory interleukin expression, excessive nitric oxide and prostaglandin generation, and the disturbances in NFκB and MAPK signaling cascades [15,16,17,18]. Pathogen-induced inflammation is associated with an increase in Reactive Oxygen Species (ROS) and Reactive Nitrogen Species (RNS) production and the activation of the inflammatory response depletes tissue antioxidants and exposes the host to increased risk of oxidative stress [21, 22]
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