Involvement of the anti-inflammatory, anti-apoptotic, and anti-secretory activity of bee venom in its therapeutic effects on acetylsalicylic acid-induced gastric ulceration in rats. (1st May 2019)

• Record Type: Journal Article
• Authors: Mohamed, Wafaa A.; Abd-Elhakim, Yasmina M.; Ismail, Shimaa A.A.
• Is Part Of: Toxicology. Volume 419(2019)
• Page Start: 11
• Page End: 23
• Publication Date: 2019-05-01
• Subjects: Bee venom -- Acetylsalicylic acid -- Gastric ulcer -- Oxidative stress -- Inflammation -- Apoptosis; Toxicology -- Periodicals; Chemicals -- Physiological effect -- Periodicals; 615.9005
• DOI: 10.1016/j.tox.2019.03.003
• Languages: English
• ISSNs: 0300-483X

Abstract

Highlights: Bee venom (BV) reduced acetylsalicylic acid (ASA)-induced pro-inflammatory cytokines release. BV adjusted caspase-3, BAX, and Hsp70 ASA-induced expression in gastric tissue. BV reduced ASA- induced oxidative stress and lipid peroxidation. BV corrected ASA- induced hematological and hemostatic alterations. BV could be a candidate therapy for ASA-induced gastric ulceration. Abstract: Acetylsalicylic acid (ASA) is the most highly consumed pharmaceutical product worldwide. Importantly, gastrointestinal ulceration due to ASA is a major complication. Hence, the present work aimed to examine, for the first time, the healing properties of bee venom (BV) in acute gastric ulceration induced by ASA. Forty adult male Sprague-Dawley rats were divided into four groups that received distilled water only, ASA (500 mg/kg BW) twice daily for 3 days, ASA for 3 days followed by BV (2 mg/kg BW) for 7 days, or ASA for 3 days followed by ranitidine hydrochloride (50 mg/kg BW) for 7 days. Haematological analysis, haemostatic evaluation, and inflammatory marker estimation were performed. Rat stomachs were collected for ulcer scoring, gene expression analysis, oxidative stress assays, histopathological and immunohistochemical examinations, and tissue eosinophil scoring. The results revealed that BV markedly decreased the ulcer index, pro-inflammatory cytokine levels, malondialdehyde levels, BAX distribution, caspase-3 expression, and tissue eosinophil levels. Additionally, significant increases in antioxidant enzymes and heat shock protein 70 localization in gastric tissue were evident following BV treatment after ASA exposure. Also, BV has been found to attenuate the haematological, haemostatic, and histopathological alterations induced by ASA. Our findings collectively indicate that the gastroprotective effect of BV against ASA-induced ulceration in rats is mediated by its antioxidant, anti-inflammatory, anti-apoptotic, and anti-secretory properties.