| Abstrakt: |
Introduction: Alzheimer’s disease (AD) is belonged to neurodegenerative disorder, and along with progressive findings obtained from AD pathogenesis, current therapeutic procedures provide only modest action on cognitive disturbances. However, intense interest has been made on plant-derived compounds which exert particularly powerful effect on anxiety, learning, and memory. Here we examined the effect of quercetin on anxiety like behavior, NORM, and corticolimbic structure changes in BDNF expression in scopolamine induced AD like condition in stressed rats. Methodes and Materials: Adult male Wistar rats (200-220 gr) were randomly divided into four groups (n=8 per group) including control, quercetin, scopolamine, and quercetin+scopolamine. Animals were administered orally with quercetin (40 mg/kg, 0/5 cc) and same volume of saline for 30 days. During the 21th– 30th day, 1 mg/Kg scopolamine was administered through intraperitoneal injection to rats. Experimental animals were tested in the light phase by using the open field and novel object recognition memory test. The BDNF levels in the hippocampus was evaluated by ELIZA method. Data were analyzed using Graph Pad prism version 8- and two-way ANOVA test, represented as the mean ± SEM, P<0/05 were considered statistically significant. Results: Oral exposure to quercetin, significantly decreased anxiety-like behaviors and improved NORM test (both, P=0/001). Furthermore, long lasting exposure to quercetin altered the BDNF expression in the hippocampus (P=0/01). Also, scopolamine induced anxiety like behaviors and memory impairment were improved in rats prior treated with quercetin and this was significant (P=0/01). Conclusion: Our finding demonstrates that quercetin could improve cognitive impairments induced by scopolamine. Also, quercetin displays a strong effect on hippocampus BDNF levels in AD like model. Given that BDNF plays a significant role in memory enhancement, and quercetin effects on memory and anxiety it could be a promising compound to treat cognitive impairment in dementia. [ABSTRACT FROM AUTHOR] |
