Protective Effect of Rutaecarpine in Streptozotocin-Induced Diabetes Cataracts Through the Inhibition of Aldose Reductase Activity in Male Albino Rats

International Journal of Pharmacology
2023.0

Abstract

Background and Objective: Diabetes mellitus (DM) is a major metabolic disease which affect the millions of people worldwide. The DM induces the several associate diseases like cataract, renal and hepatic failure. The main enzyme aldose reductase during the polyol pathway serves an important part in the formation of cataracts in diabetic conditions. Rutaecarpine (RT), which is an indolopyridoquinazoline alkaloid and principal compound of evodia shows therapeutic activity against several chronic illnesses. It is proven to be effective in the treatment of diabetes mellitus via altering oxidative stress and inflammation. The goal of current research was to scrutinize the pharmacological action of rutaecarpine in streptozotocin-induced diabetic cataracts in rodents. Materials and Methods: All the animals were divided into five groups and streptozotocin-induced diabetic rats were supplemented with different doses of rutaecarpine. The formation of cataracts was evaluated using the scoring technique by observer and lens digital picture. Other biochemical parameters were also assessed such as blood, insulin, blood glucose, body weight, sorbitol content, protein carbonyl content, mRNA and expression of aldose reductase in each group of rats. We also measured the kinetics properties of aldose reductase. Results: Administration of rutaecarpine alters all biochemical parameters compared to diabetic cataract rats. Rutaecarpine significantly stuck the formation of cataracts in the rats in a dose-dependent manner. The kinetic properties of aldose reductase i.e., Vmax, Km and Ki had also attenuated in diabetic cataract rats as well as mRNA and protein expression. Conclusion: Collectively, we can say that rutaecarpine has the potential to reduce the progression of cataracts in a diabetic case via the reduction of aldose reductase.

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