ABSTRACT
Background: Aluminum a known neuro and cholinotoxin has been implicated in the pathogenesis ofAlzheimer’s disease. Its exposure is associated with impairment of the memory and cognition.Objective: The present study was undertaken to evaluate the anti-Alzheimer’s activity of Vitis vinifera inaluminum induced Alzheimer’s disease.Materials and methods: In this study, we investigated the behavioral and biochemical effects ofaluminum in Sprague-Dawley rats. Animals were exposed to aluminum chloride (100 mg/kg/day) orallyfor a period of 8 weeks. Vitis was given in doses of 250 mg/kg and 500 mg/kg for 16 weeks and thepossible effects of Vitis vinifera on the expression of Tau and amyloid precursor protein were evaluated byPCR analysis and the possible activities of lipid peroxidation, inflammation and anti-cholinesterase activity were evaluated.Results: Aluminum intoxication was associated with significant impairment in learning and memory inMorris water maze test. A significant improvement was observed with Vitis vinifera in a dose dependentmanner.Conclusion: The findings of the present study revealed the significant neuroprotective actions of Vitisvinifera by modifying the biochemical parameters and inhibited the mRNA expression of Amyloid Precursor Protein and Tau, which are the key pathological hallmarks of Alzheimer’s disease, which wasfurther confirmed by histopathological observations.© 2017 Transdisciplinary University, Bangalore and World Ayurveda Foundation. Publishing Services byElsevier B.V. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
ABSTRACT
Reperfusion injury is remarkable clinical issue that needs to be resolved as ischemia-reperfusion is a common phenomenon encountered in numerous clinical situations. The present communication report the involvement of nitric oxide (NO) in cardioprotection offered by flavonoids (rutin and quercetin) against myocardial ischemia reperfusion. Rutin produced better cardioprotection than quercetin in normal and diabetic rats. The observed cardioprotection offered with quercetin and rutin was partially abolished by prior administration of nitric oxide synthase inhibitor, L-NAME (N-nitro-L-arginine methyl ester) in both normal and diabetic rats. L-NAME abolished the cardioprotective actions of rutin more strongly than the cardioprotective actions of quercetin. However, mechanistic study with NOS inhibitor implied the possible partial role of nitric oxide in infarct size limiting effect of quercetin and rutin.