BackgroundWe aimed in the present study, at investigating the gastroprotective effect of carob pods aqueous extract (CPAE) against ethanol-induced oxidative stress in rats as well as the mechanism implicated.MethodsAdult male wistar rats were used and divided into six groups of ten each: control, EtOH (80 % v/v, 4 g/kg b.w.), EtOH 80 % + various doses of CPAE (500, 1000 and 2000 mg/kg, b.w.) and EtOH + Famotidine (10 mg/kg, p.o.) Animals were perorally (p.o.) pre-treated with CPAE during 15 days and intoxicated with a single oral administration of EtOH (4 g/kg b.w.) for two hours.ResultsThe colorimetric analysis demonstrated that the CPAE exhibited an importance in vitro antioxidant activity against ABTS and DPPH radicals. We found that CPAE pretreatment in vivo, protected against EtOH-induced macroscopic and histological changes induced in stomach mucosa. Carob extract administration also protected against alcohol-induced volume gastric juice decrease. More importantly, We showed that CPAE counteracted EtOH-induced gastric lipoperoxidation, reversed the decrease of sulfhydryl groups (−SH) an hydrogen peroxide (H2O2) levels, and prevented the depletion of antioxidant enzyme activity of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx).ConclusionsThese findings suggest that CPAE exerted a potential gastro-protective effect against EtOH-induced oxidative stress in rats, due in part, to its antioxidants properties.
BackgroundMassive alcohol drinking can lead to gastric ulcer. In the present study we investigated the gastroprotective effect of Citrus sinensis peel aqueous extract (CSPE) and Hesperidin (H) in ethanol (EtOH) induced oxidative stress and peptic ulcer in rats.MethodsSeventy adult male Wistar rats were divided into seven groups of 10 each: control, EtOH (4 g/kg b.w.), EtOH + various doses of CSPE (100, 200 and 400 mg/kg, b.w.), EtOH + Hesperidin (50 mg/kg, p.o.) and EtOH + Omeprazole (OM, 20 mg/kg, p.o.). Animals were perorally (p.o.) pre-treated with CSPE during 15 days and intoxicated with a single oral administration of EtOH (4 g/kg b.w.) during 2 h. Gastric ulcer was induced in rats with a single dose of ethanol (EtOH). Ulcer index, gene expression of gastric cyclooxygenase-2 (COX-2), tumor necrosis factor alpha (TNF-α), malondialdhyde (MDA), hydrogen peroxide H2O2 and Thiol groups (−SH) content in stomach and antioxidant enzymes superoxide dismutase (SOD), catalase (CAT) and gluthation peroxidise (GPx) were measured. Furthermore, histopathological examinations were performed.ResultsThe results showed that ethanol induced gastric damage, improving oxidative stress markers level such as MDA (121 ± 4.45 nmol/mg proteins) and H2O2 (24.62 ± 1.04 μmol/mg proteins), increased pro-inflammatory cytokine (TNF-α level), as well as the expression of COX-2 in the ethanol group. However, a significant depletion of enzymatic and non-enzymatic antioxidants were observed, such as, GPx (72%), SOD (57.5%), CAT (41.6%) and -SH (50%). The lesions were associated with severe histopathological damage. The both Citrus sinensis peel aqueous extract (CSPE) and hesperidin significantly protect against all gastric damages caused by ethanol administration in rats.ConclusionsWe propose that CSPE and hesperidin exhibit protective effects in EtOH-induced peptic ulcer in rat. This protection might be related in to part its antioxidant properties as well as its opposite effects on some studied intracellular mediators.
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