ABSTRACT
ABSTRACT Objective: To investigate the protective effect of wolfberry (WB) against acetic acid-induced colitis in rats. Methods: The rats were divided into four groups with eight rats in each group: the control group, WB group, colitis group and WB + colitis group. Distal colitis was induced in rats by intracolonic instillation of 4% acetic acid. Wolfberry + colitis group received 100 mg/kg of WB extract dissolved in saline through the intraperitoneal route for 7 days. Acute colitis was created on the 8th day, and the rats were sacrificed 48 hours later. Colonic damage was assessed by macroscopic and histological criteria as well as biochemical markers. Results: Mean total antioxidant capacity (TAC), total oxidant status (TOS), tumour necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6 levels were significantly higher in the colitis group compared with the control and WB groups (p < 0.05). The WB + colitis group had significantly lower TAC, TOS, TNF-α, IL-1β and IL-6 levels compared with the colitis group (p < 0.05). The analyses of the histopathological findings indicated that the colitis group had a significantly higher histopathological damage score than the control group (3.12 ± 0.45, 0 ± 0.00, respectively; p < 0.05). Histopathological damage score was significantly higher in the WB + colitis group than in the control group and statistically significantly lower than the colitis group (1.62 ± 0.44, 0 ± 0.00, respectively; 3.12 ± 0.45, respectively; p < 0.05 for both comparisons). Conclusion: Wolfberry extract is an agent that is effective for preventing acetic acid-induced colitis in rats.
ABSTRACT
ABSTRACT Objective: Ethyl alcohol (EA) is a substance that is used commonly worldwide and known to have toxic effects on the liver. The aim of this study was to investigate the effect of montelukast sodium (MK) on acute hepatopathy induced by a single dose of EA in rats. Methods: The study consisted of four groups each containing eight Wistar albino male rats. The groups were classified as follows: the control group received distilled water; the EA group received 6 g/kg EA diluted with distilled water orally by gavage; the MK group received 30 mg/kg MK orally by gavage; the EA + MK group received, 2 hours after the EA administration, ie 30 mg/kg MK orally by gavage. After 24 hours, all the rats were sacrificed, and their blood and liver tissue samples were taken for biochemical and histopathological examinations. Results: The administration of EA caused a statistically significant increase in aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels compared with the control group (220.50 ± 66.90 and 92.38 ± 5.90 versus 84.88 ± 15.66 and 43.75 ± 10.22). The administration of EA + MK caused a statistically significant decrease in the AST and ALT levels compared with the EA alone group. Ethyl alcohol administered to the rats caused lesion in the liver including congestions, hydropic degeneration and irregular shaped area caused coagulation necrosis. The histopathological changes seen in the EA group were not detected in the EA + MK group. Conclusion: Consequently, these data suggested that MK had beneficial effects in alleviating EA-induced hepatotoxicity in rats.