Nicotinamide is being used in experimental and clinical trials examining the prevention of type-1 diabetes mellitus. However, the precise mechanisms underlying the antidiabetic and neuroprotective effects of nicotinamide require further analysis. Our goals are to evaluate the protective effect and the cellular and molecular mechanisms of nicotinamide against brain damage induced by type-1 diabetes in rats. Type-1 diabetes was induced by i.p injection of streptozotocin (50 mg/kg). Ten days after the induction of diabetes, rats were divided into two groups, control diabetic group and nicotinamide-treated group. Nicotinamide was i.p administered at daily dose of 100 mg/kg for a period of 4 weeks. Another group of normal animals was served as normal control group. The diabetic group showed a significant (p < 0.05) decrease in the content of brain DNA, RNA and glutathione, whereas, the contents of lipid peroxide, as malondialdehyde, and nitric oxide were significantly increased. The activities of aldose reductase, sorbitol dehydrogenase and cytochrome oxidase were significantly increased, whereas, the activities of glutathione reductase, glutathione peroxidase, glutathione-S-transferase and superoxide dismutase were significantly decreased. Nicotinamide administration produced restoration of brain malondialdehyde, nitric oxide, glutathione, RNA, DNA levels and the activities of the most measured enzymes. In conclusion, nicotinamide could ameliorate brain damage induced by type-1 diabetes in Wistar rats. The present data provide new approaches for the precise cellular and molecular mechanisms of the neuroprotective effect of nicotinamide.
Key words: Nicotinamide, STZ-diabetes, rat brain, polyol pathway, oxidative status, antioxidant systems, DNA and RNA levels.
Copyright © 2021 Author(s) retain the copyright of this article.
This article is published under the terms of the Creative Commons Attribution License 4.0