Biochemical and histopathological study of the anti-hyperglycemic and anti-hyperlipidemic effects of cornelian cherry (Cornus mas L.) in alloxan-induced diabetic rats.

BACKGROUND

Anthocyanins are phytochemicals with a multitude of pharmacological actions including anti-diabetic and anti-hyperlipidemic effects. This study was undertaken to evaluate the anti-hyperglycemic and anti-hyperlipidemic effects of cornelian cherry (Cornus mas L., CM) fruits - that are rich in anthocyanins and known to have medicinal properties- in alloxan-induced diabetic rats.

METHODS

Twenty-eight adult male rats were randomly assigned to four groups of seven animals each: non-diabetic control, diabetic control, glibenclamide-treated (0.6 mg/kg/day; 4 weeks) and CM fruit-treated (2 g/day; 4 weeks) group. Diabetes was induced by a single injection of alloxan (120 mg/kg). Fasting serum levels of glucose, total cholesterol (TC), low- (LDL-C) and high-density lipoprotein cholesterol (HDL-C), triglycerides (TG), aspartate (AST) and alanine aminotransferase (ALT) and alkaline phosphatase (ALP) were measured at the end of study period.

RESULTS

Diabetic rats had significantly elevated levels of serum glucose, LDL-C, TG, AST, ALP and ALT and decreased levels of HDL-C compared to the non-diabetic group (p<0.05). Treatment with either glibenclamide or CM counterbalanced the above-mentioned abnormalities. The effects of CM were comparable to those of glibenclamide at the doses tested in this study. Serum glucose, TG, ALP and HDL concentrations in the normal group were significantly changed compared to the diabetic control group (p<0.05). There were no significant changes in evaluated biochemical parameters between the glibenclamide and CM groups with normal group. Histopathological examinations revealed a less severe hepatic portal inflammation in the CM-treated vs. other study groups.

CONCLUSIONS

Dietary supplementation with CM fruits effectively prevents the development of diabetes mellitus, dyslipidemia and hepatic inflammation in alloxan-induced diabetes.