ABSTRACT
Background and Aim: Based on recent studies, atorvastatin has some pleiotropic actions such as anti-inflammatory and anti-oxidant effects independent of lipid lowering effects. Regarding the critical role of oxidative stress and inflammation in inducing diabetic neuropathy, the current study aimed at examining the neuroprotective and anti-oxidative stress effects of atorvastatin at the brain tissues in diabetes experimental models
Materials and Methods: Twenty-four male Wistar rats were randomly divided into 4 equal groups including normal, normal treated, diabetic and diabetic treated. The diabetic group were made diabetic by an intravenous injection of streptozotocin [40mg/kg] and the treated group received 40mg/kg/day atorvastatin for 8 weeks. At the end of the experiment, blood samples from the subjects were derived to measure their blood glucose and urea. Finally, the rats were killed under deep anesthesia and their brains were removed in order to measure malondialdehyde [MDA] and to make histopathological assessment
Results: Uncontrolled hyperglycemia [blood glucose >450 mg/dl] significantly increased blood urea in the diabetic group [130 +/- 10 mg/dl] compared with the normal group [58 +/- 7 mg/dl], [P<0.05]. Also, hyperglycemia increased brain MDA of the diabetic group [8.78 +/- 3.07micromol/mg protein] associated with histopathological damages. Atorvastatin significantly decreased blood urea of the diabetic rats [76 +/- 5 mg/dl] accompanied by histopathological damages. Finally, the content of brain MDA significantly decreased in diabetic rats treated with atorvastatin [0.92 +/- 0.31micromol/mg protein], [P<0.05]
Conclusion: The findings of the present study reveal that atorvastatin is able to prevent hyperglycemia-induced diabetic neuropathy and inhibit brain oxidative stress during diabetes. It is probable that reduction of urea is one of the reasons for atorvastatin prevention of hyperglycemia-induced neuropathy