Objectives: The modulation of vascular endothelial growth factor, antioxidants, and tissue necrosis factor alpha (TNF-α) using ethanol stem bark extract of Boswellia dalzielii H. was evaluated in an ethanol-induced gastric ulcer albino rat model.
Methods: Thirty albino rats of either sex (200–250 g) were starved for 48 h but were allowed drinking water with 8% sucrose to avoid dehydration. The rats were placed on wire gauze above the base of the cage to prevent coprophagy. At the end of the fasting period, the rats were equally divided and assigned to six treatment groups. Group A served as control and 5 ml/kg distilled water was orally administered to the rats without further treatment. Rats in group B were given 5 ml/kg distilled water and served as negative control. Rats in groups C, D, and E were pretreated with 100, 200, and 400 mg/kg of the ethanol stem bark extract of B. dalzielii H, respectively. Group F received 50 mg/kg ranitidine. After 1 h, all the rats in groups B–F were each given absolute ethanol 1 ml/200 g body weight of rat. All treatments were by intragastric lavage. One hour after the treatment with ethanol, all the rats in the experiment (groups A–F) were euthanized with an overdose of anesthetic ether and their stomachs were excised. The stomachs were cut along the greater curvature and washed in warm normal saline. Each stomach was stretched out and pinned on board.
Results: The results of the study revealed that pretreatment with ethanol stem bark extract of B. dalzielii H. decreased gross and histological gastric mucosal damage caused by intragastric administration of absolute ethanol in a dose-dependent manner when compared with controls. The gastric ulcer index and gastric tissue level of malondialdehyde (MDA) and TNF-α were significantly reduced (p<0.001), whereas the gastric tissue level of superoxide dismutase, catalase, total antioxidant capacity, and vascular endothelial growth factor (VEGF) was significantly increased (p<0.001) when compared with the controls.
Conclusion: The plant extract attenuated gastric mucosal damage induced by ethanol via upregulation in the expression of gastric tissue VEGF, reinforcement of the antioxidant system, and reduction in the gastric tissue level of MDA and the pro-inflammatory cytokine TNF-α.