Hydroxyquinoline sulfanilamide ameliorates STZ-induced hyperglycemia-mediated amyleoid beta burden and memory impairment in adult mice

Abstract

The aim of the current study was to evaluate therapeutic potentials of Hydroxyquinoline Sulfanilamide (HSM) for Alzheimer’s disease in a mice model of Streptozotocin (STZ)-induced diabetes. The antioxidant analysis of mice brain homogenates was carried out by catalase (CAT) assay, reduced glutathione (GSH) assay, and lipid peroxidation (LPO) assay. Biochemical analysis of blood plasma was conducted by peroxidase (POD) assay and superoxide dismutase (SOD) assay. The expression of mice brain proteins was evaluated using Western Blotting analysis. The administration of HSM increased the activity of antioxidant enzymes including CAT, SOD, GSH, and POD and lowered LPO actions. These findings indicate that STZ may lead to diabetes in mice, followed by hypercholesterolemia, expressed as triglycerides in mice blood. However, HSM significantly decreased STZ-induced hyperglycemia and hypercholesterolemia in adult albino mice. The data confirmed that HSM lowered STZ-induced oxidative stress, inhibited phosphorylated JNK, NF-kB, and upregulated Nrf-2 to improve and restore the synapse and memory defects in adult albino mice. Conclusively, the current findings suggested that HSM is a safe, novel, and potential drug candidate against metabolic dysfunction and induced cognitive impairment.

Keywords

• diabetes mellitus
• streptozotocin
• neuroinflammation
• morris water maze
• hydroxyquinoline sulfanilamide