Dose Dependent Hepatic and Endothelial Changes in Rats Treated with Dexamethasone.

AIMS AND OBJECTIVES: To study the effect of dexamethasone on liver and endothelium, and to determine the optimum dose which induces the abnormal changes in liver and endothelium in Wistar rats. MATERIALS AND METHODS: Albino Wistar rats were divided into 7 groups (n=6). Control group rats received normal saline. Graded doses of dexamethasone (0.5,1,2,4,8 and 16mg/kg/ i.p.) was administered to the groups for six days. Liver and aorta were dissected at the end of the study and examined for histopathological changes under microscope. RESULTS: Intraperitoneal administration of dexamethasone (4,8 and 16mg/kg) for six days resulted in fatty changes in liver and same doses have shown thickening of endothelial layers in aorta, in comparison to control group. There were not much significant changes seen in low doses of dexamethasone (0.5, 1 and 2mg/kg). CONCLUSION: It is concluded that the acute high doses of dexamethasone (4,8 and 16mg/kg) for six days caused hepatic steatosis and showed mild to moderate arteriosclerosis in aorta. These changes may be secondary consequences of insulin resistance. Hence, it can be used as new animal model to screen the various plants and medicines in the treatment of insulin resistance.

Evaluation of antiulcerogenic potential of antioxidant α-tocopherol in pylorus-ligated albino rats.

BACKGROUND: Oxidative free radicals and lipid peroxidation mediate gastric injury. α-Tocopherol is a redox agent with biological and antioxidant property, hence, may provide ulcer protection. METHODS: Pylorus-ligated Shay rats (n=6) were used as the experimental gastric ulcer animal model. The rats were divided into three groups. Group I received saline (5 mL/kg), Group II α-tocopherol (12.5 mg/kg), and Group III omeprazole (3.6 mg/kg), orally daily for 5 days prior to ulcerogenic challenge. Nineteen hours after the challenge, the rats were sacrificed and their stomachs isolated and studied for degree of gastric injury. Formed gastric juice was collected for measurement of volume, titrimetric estimation of free and total acidity, and total acid output by the conventional methods. The ulcer index and total acid outputs were calculated. RESULTS: α-Tocopherol exerted significant (p<0.05) antiulcer activity (the ulcer index was reduced to 7.4 ± 1.0 from the control value of 19.8 ± 4.1). α-Tocopherol also significantly reduced free and total acidity, gastric juice volume, and total acid output (p<0.01). The results were analyzed by ANOVA and Scheffe's multiple comparison test. CONCLUSIONS: The study demonstrates that α-tocopherol has significant antiulcer activity. It, perhaps, acts by decreasing hydrochloric acid output.

Silymarin, an antioxidant bioflavonoid, inhibits experimentally-induced peptic ulcers in rats by dual mechanisms.

INTRODUCTION: Antioxidants are reported to have antiulcer activity. We investigated silymarin, a bioflavonoid antioxidant, for antiulcer potential. MATERIALS AND METHODS: Pylorus-ligated Shay rats (n=5) were used as the experimental gastric ulcer animal model. The rats, separated into three groups, were administrated silymarin (50 mg/kg), omeprazole (3.6 mg/kg), or saline (5 ml/kg) per orally daily for 5 days prior to ulcerogenic challenge. Nineteen hours after the challenge, the rats were sacrificed and their stomachs isolated. Formed gastric juice was collected for measurement of volume, titrimetric estimation of free and total acidity, and total acid output by the conventional methods. The ulcer index was calculated. Total acid output and free and combined acid quantities were calculated using the acidity value and the volume of formed gastric juice. RESULTS: Silymarin exerted significant (P<.05) antiulcer activity (the ulcer index was reduced to 7.4 ± 1.0 from the control value of 19.8 ± 4.1). Silymarin also significantly reduced free and total acidity, gastric juice volume, total acid output, and combined acid content. The results were analyzed by ANOVA and Newman-Keuls multiple comparison test. CONCLUSION: This study demonstrates that silymarin has significant antiulcer activity. It perhaps acts by decreasing hydrochloric acid output and increasing buffering power (combined acid).