Paper Report for: Xianchu_2022_Pak.J.Pharm.Sci_35_769

Diabetes is a well-known risk factor for cognitive deficit. Rutin (RUT) possesses diverse pharmacological activities and is widely used in diabetic complication. The aim of this study is to assess the improvement of RUT on diabetes-associated cognitive decline (DACD). In our study, Morris water maze was examined to estimate cognitive function. In hippocampus tissue, spectrophotometer was performed to evaluate super oxide dismutase (SOD), catalase (CAT), reduced glutathione (GSH), malondialdehyde (MDA), acetyl cholinesterase (AChE) and choline acetyl transferase (ChAT) levels. Quantitative real-time polymerase chain reaction (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA) were utilized to analyze Tumor necrosis factor-a (TNF-a) and interleukin-1beta (IL-1beta) contents. Western blot was used to detect the protein expressions of brain derived neurotrophic factor (BDNF), glial fibrillary acidic protein (GFAP), nuclear factor erythroid-2-related factor-2 (Nrf-2) and heme oxygenase-1 (HO-1). Our data revealed that RUT markedly improved learning and memory capacities in Morris water maze test. In hippocampus, RUT markedly inhibited AChE, GFAP MDA, TNF-a and IL-1beta levels and augmented ChAT and BDNF, SOD, CAT, GSH, Nrf-2 and HO-1 levels. In conclusion, RUT may be involved in protection efficacy against STZ-induced cognitive deficits via improvement of oxidative stress, inflammatory response and Nrf-2/HO-1 pathway.