Please use this identifier to cite or link to this item: http://10.1.7.192:80/jspui/handle/123456789/12027
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dc.contributor.authorDeshmukh, Pankaj S.-
dc.date.accessioned2023-11-04T08:01:09Z-
dc.date.available2023-11-04T08:01:09Z-
dc.date.issued2023-05-
dc.identifier.urihttp://10.1.7.192:80/jspui/handle/123456789/12027-
dc.description.abstractBackground: Alzheimer's disease (AD) is a neurological condition affecting older individuals. Targeting beta amyloid formation has produced inconsistent results. β-amyloid accumulation disrupts calcium control, leading to issues like tau hyperphosphorylation and autophagy inhibition. The Cav1.2 subtype of L-type calcium channel is involved in memory and synaptic plasticity. Calcium channel blockers (CCBs) are being investigated as a potential treatment for AD. CCBs can reduce the formation of Aβ oligomers by blocking calcium influx through L-type channels, potentially reducing toxicity. They also inhibit inflammation and oxidative stress. Overall, CCBs have the potential to enhance cognition and improve memory in AD. Aim & Objective: The purpose of the study was to evaluation of neuroprotective effect of barnidipine against streptozotocin induced Alzheimer’s disease model in rats. Material & Methods: Forty-two female Wistar rats weighing 350 ± 10 g were divided into seven groups: NC (Normal Control), SH (Sham Control), DC (Disease Control), Dono-5 (Disease Treatment with Donepezil), Bar-1, Bar-2, and Bar-5 (Disease Treatment with Barnidipine). Each group had six animals and the treatments lasted for 21 days. Cognitive function and behavior were assessed using modified Y-maze and novel object recognition tests after 21 days. Biochemical estimation, histopathological and immunohistochemical examination, were performed. Results: Barnidipine treatment significantly improved exploratory behavior and object discrimination compared to the disease control group. Protein metabolism was altered, with decreased total protein levels in the treatment group. Antioxidant capacity was enhanced with elevated glutathione levels and oxidative stress was reduced with lower MDA levels. Inflammatory markers showed a reduction, indicating a potential attenuation of the inflammatory response. Histopathological analysis showed a reduction in senile plaques and neurodegeneration, suggesting a therapeutic effect on AD-associated pathology Conclusion: Barnidipine treatment showed potential beneficial effects in cognitive functions, neuroprotective markers, and reduction in senile plaques. Bar-2 group demonstrated the best results. This data provides a basis for further research and development.en_US
dc.publisherInstitute of Pharmacy, Nirma University, A'baden_US
dc.relation.ispartofseriesPDR00800;-
dc.subjectDissertation Reporten_US
dc.subjectPharmacologyen_US
dc.subject21MPHen_US
dc.subject21MPH210en_US
dc.subjectPDR00800en_US
dc.titleEvaluation Effect of Bamidipine in Streptozotocin Induced Alzheimer's Disease Model in Ratsen_US
dc.typeDissertationen_US
Appears in Collections:M.Pharm. Research Reports, Department of Pharmacology

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