Kalayanaka ghrita Ameliorates Okadaic Acid Induced Memory Deficits in Wistar Rats
Authors
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Department of Pharmacology, Bharati Vidyapeeth (Deemed to be University), Poona College of Pharmacy, Pune – 411038, Maharashtra ,IN
Diddi Sneha Latha -
Department of Pharmaceutical Chemistry, Bharati Vidyapeeth (Deemed to be University), Poona College of Pharmacy, Pune – 411038, Maharashtra ,INSathiyanarayanan Lohidasan
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Department of Pharmacology, Bharati Vidyapeeth (Deemed to be University), Poona College of Pharmacy, Pune – 411038, Maharashtra ,INArulmozhi S.
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Department of Pharmaceutical Chemistry, Bharati Vidyapeeth (Deemed to be University), Poona College of Pharmacy, Pune – 411038, Maharashtra ,INKakasaheb R. Mahadik
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Regional Ayurveda Institute for Fundamental Research, CCRAS, Ministry of AYUSH, Pune – 411038, Maharashtra ,INShrirang Jamadagni
DOI:
https://doi.org/10.18311/jnr/2024/44982Keywords:
Alzheimer’s Disease, Brain Monoamines, Kalyanaka ghrita, Neuroprotection, Okadaic AcidAbstract
Background: Alzheimer’s disease depicts the characteristic features of intracellular neurofibrillary tangles and extracellular amyloid plaques. Kalyanaka ghrita (KG) is an Ayurvedic formulation used to treat impaired learning and memory such as Manasmandata or Buddhimandyata. KG is traditionally used to enhance memory. The constituents present in KG are also reported to be memory-enhancing, anti-inflammatory, and antioxidant and KG is reported to be effective in neurodegeneration in rats induced by β-amyloid. Aim: This study is aimed to validate the effect of KG on memory deficit, tauopathy and neurodegeneration induced by intracerebroventricular administration of okadaic acid. Methods: Okadaic acid was administered intracerebroventricularly on day 7 to the Wistar rats. KG was administered orally or intranasal from day 14 to 35 to the respective groups. The behavioural parameters on spatial memory, social recognition, and novel object recognition tests were determined. The molecular parameters such as brain acetylcholinesterase activity, protein phosphatase 2A, antioxidant parameters, monoamine levels and the brain histopathology were studied. Results: KG treatment significantly improved cognition, as evidenced by a decrease in escape latency, path length, and social and novel object recognition tests. KG treatment also increased the brain Protein phosphatase 2A, reversed the oxidative stress, and decreased brain acetylcholinesterase. The brain monoamines were reversed upon treatment with KG. Further, the molecular and histological studies confirmed the prevention of neuronal damage. Conclusion: These findings imply the traditional nootropic property of KG. The neuroprotective properties and decreased neurofibrillary tangles upon treatment with KG suggest KG to be a potential therapy for AD-like neurodegeneration.
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Copyright (c) 2024 Sneha Diddi, Arulmozhi S, Sathiyanarayanan Lohidasan, Kakasaheb R. Mahadik, Shrirang Jamadagni (Author)
This work is licensed under a Creative Commons Attribution 4.0 International License.
Accepted 2024-09-04
Published 2024-11-06
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