Abstract
Gastric ulcer has shown association with changes in sex hormones, with impact exacerbated in males. Also, males are known to be more exposed to ulcer risk factors. This study investigates the effect of testosterone on indomethacin induced gastric ulcers in adult female rats. Eighteen female rats (225 ± 25 g body weight) were randomly assigned to 3 groups under standard laboratory condition. After acclimatization, animals fasted for 40 hrs but were given waterad libitum. Group A served as control while group B served as the ulcer control, in which ulcer was induced without treatment using indomethacin (40 mg/kg single orally dose). Group C was pretreated with testosterone (1 mg/kg IM) eight hours before ulcer induction. Eight hours after ulcer induction, animals were sacrificed and the stomach was harvested for analysis. Results showed a significant reduction in mucus content in groups C (0.79±0.11 g) and B (0.87±0.02 g) compared to A (1.11±0.03 g). Gastric mucus pH was significantly acidic in group B (4.40±0.55) compared to C (5.20±0.45) and A (5.80±0.45). There was a significantly higher ulcer index in group B (4.60±0.55 mm) compared to C (3.60±0.89 mm) and testosterone pretreatment resulted in a 21.74% ulcer inhibition. Although weak, the findings suggest that testosterone might protect the gastric mucosa against NSAIDs in females.
Highlights
Nonsteroidal anti-inflammatory drugs (NSAIDs) have long been implicated in ulcer aetiology and employed in several animal studies for gastric ulcers induction [1,2,3,4]
Gastric ulcerogenic action of NSAIDs is reported to be due to their local inhibitory effect on gastric prostaglandin E2 (PGE2) and prostaglandin I2 (PGI2) that are the main inhibitors of gastric acid secretion [7] as well as induction of osmotic lysis subsequent to trapping of charged NSAIDs with the epithelial cells [8] and death of the epithelial cell subsequent to uncoupling of oxidative phosphorylation [9]
This study investigates the protective effect of testosterone on indomethacin induced gastric ulcer in female rats
Summary
Nonsteroidal anti-inflammatory drugs (NSAIDs) have long been implicated in ulcer aetiology and employed in several animal studies for gastric ulcers induction [1,2,3,4]. Indomethacin is a commonly used type of NSAIDs in animal experiment whose proposed mechanism of stomach damage has been reported to be through local/topical and systemic actions. The development of peptic ulcer has been said to be influenced by various aggressive and defensive factors [13,14,15], inadequate dietary habits, cigarette smoking, excessive ingestion of nonsteroidal anti-inflammatory agents, stress, hereditary predisposition, Helicobacter pylori infection [1, 3, 16,17,18], free radicals formation [19], and decreased prostaglandin synthesis [20]. There is a growing interest in alternative therapies with promising outcomes and nontoxic effects to other organs or systems
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