Kolaviron neuroprotective effect against okadaic acid-provoked cognitive impairment
Alzheimer's disease (AD) is acknowledged as the main causative factor of dementia that affects millions of people around the world and is increasing at increasing pace. Okadaic acid (OA) is a toxic compound with ability to inhibit protein phosphatases and to induce tau protein hyperphosphorylat...
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Format: | Article |
Language: | English |
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Elsevier
2024-02-01
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Series: | Heliyon |
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Online Access: | http://www.sciencedirect.com/science/article/pii/S2405844024015950 |
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author | Morteza Nazari-Serenjeh Tourandokht Baluchnejadmojarad Masoud Hatami-Morassa Javad Fahanik-Babaei Soraya Mehrabi Mahsa Tashakori-Miyanroudi Samira Ramazi Seyed-Mahdi Mohamadi-Zarch Davood Nourabadi Mehrdad Roghani |
author_facet | Morteza Nazari-Serenjeh Tourandokht Baluchnejadmojarad Masoud Hatami-Morassa Javad Fahanik-Babaei Soraya Mehrabi Mahsa Tashakori-Miyanroudi Samira Ramazi Seyed-Mahdi Mohamadi-Zarch Davood Nourabadi Mehrdad Roghani |
author_sort | Morteza Nazari-Serenjeh |
collection | DOAJ |
description | Alzheimer's disease (AD) is acknowledged as the main causative factor of dementia that affects millions of people around the world and is increasing at increasing pace. Okadaic acid (OA) is a toxic compound with ability to inhibit protein phosphatases and to induce tau protein hyperphosphorylation and Alzheimer's-like phenotype. Kolaviron (KV) is a bioflavonoid derived from Garcinia kola seeds with anti-antioxidative and anti-inflammation properties. The main goal of this study was to assess whether kolaviron can exert neuroprotective effect against okadaic acid-induced cognitive deficit. Rats had an intracerebroventricular (ICV) injection of OA and pretreated with KV at 50 or 100 mg/kg and examined for cognition besides histological and biochemical factors. OA group treated with KV at 100 mg/kg had less memory deficit in passive avoidance and novel object discrimination (NOD) tasks besides lower hippocampal levels of caspases 1 and 3, tumor necrosis factor α (TNFα) and interleukin 6 (IL-6) as inflammatory factors, reactive oxygen species (ROS), protein carbonyl, malondialdehyde (MDA), and phosphorylated tau (p-tau) and higher level of acetylcholinesterase (AChE) activity, mitochondrial integrity index, superoxide dismutase (SOD), and glutathione (GSH). Moreover, KV pretreatment at 100 mg/kg attenuated hippocampal CA1 neuronal loss and glial fibrillary acidic protein (GFAP) reactivity as a factor of astrogliosis. In summary, KV was able to attenuate cognitive fall subsequent to ICV OA which is partly mediated through its neuroprotective potential linked to mitigation of tau hyperphosphorylation, apoptosis, pyroptosis, neuroinflammation, and oxidative stress and also improvement of mitochondrial health. |
first_indexed | 2024-03-08T00:10:29Z |
format | Article |
id | doaj.art-c6bddcfb9dde46af823d868b73806230 |
institution | Directory Open Access Journal |
issn | 2405-8440 |
language | English |
last_indexed | 2024-03-08T00:10:29Z |
publishDate | 2024-02-01 |
publisher | Elsevier |
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series | Heliyon |
spelling | doaj.art-c6bddcfb9dde46af823d868b738062302024-02-17T06:41:27ZengElsevierHeliyon2405-84402024-02-01103e25564Kolaviron neuroprotective effect against okadaic acid-provoked cognitive impairmentMorteza Nazari-Serenjeh0Tourandokht Baluchnejadmojarad1Masoud Hatami-Morassa2Javad Fahanik-Babaei3Soraya Mehrabi4Mahsa Tashakori-Miyanroudi5Samira Ramazi6Seyed-Mahdi Mohamadi-Zarch7Davood Nourabadi8Mehrdad Roghani9Student Research Committee, Iran University of Medical Sciences, Tehran, Iran; Department of Physiology, School of Medicine, Iran University of Medical Sciences, Tehran, IranDepartment of Physiology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran; Corresponding author.Department of Physiology, School of Medicine, Iran University of Medical Sciences, Tehran, IranElectrophysiology Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, IranDepartment of Neuroscience, Faculty of Advanced Technologies in Medicine, Iran University of Medical Science, Tehran, Iran; Cellular and Molecular Research Center, Iran University of Medical Sciences, Tehran, IranPsychiatry and Behavioral Sciences Research Center, Addiction Institute, Mazandaran University of Medical Sciences, Sari, IranStudent Research Committee, Iran University of Medical Sciences, Tehran, IranDepartment of Physiology, Faculty of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, IranDepartment of Physiology, Faculty of Medicine, Tehran Medical Sciences, Islamic Azad University, Tehran, IranNeurophysiology Research Center, Shahed University, Tehran, IranAlzheimer's disease (AD) is acknowledged as the main causative factor of dementia that affects millions of people around the world and is increasing at increasing pace. Okadaic acid (OA) is a toxic compound with ability to inhibit protein phosphatases and to induce tau protein hyperphosphorylation and Alzheimer's-like phenotype. Kolaviron (KV) is a bioflavonoid derived from Garcinia kola seeds with anti-antioxidative and anti-inflammation properties. The main goal of this study was to assess whether kolaviron can exert neuroprotective effect against okadaic acid-induced cognitive deficit. Rats had an intracerebroventricular (ICV) injection of OA and pretreated with KV at 50 or 100 mg/kg and examined for cognition besides histological and biochemical factors. OA group treated with KV at 100 mg/kg had less memory deficit in passive avoidance and novel object discrimination (NOD) tasks besides lower hippocampal levels of caspases 1 and 3, tumor necrosis factor α (TNFα) and interleukin 6 (IL-6) as inflammatory factors, reactive oxygen species (ROS), protein carbonyl, malondialdehyde (MDA), and phosphorylated tau (p-tau) and higher level of acetylcholinesterase (AChE) activity, mitochondrial integrity index, superoxide dismutase (SOD), and glutathione (GSH). Moreover, KV pretreatment at 100 mg/kg attenuated hippocampal CA1 neuronal loss and glial fibrillary acidic protein (GFAP) reactivity as a factor of astrogliosis. In summary, KV was able to attenuate cognitive fall subsequent to ICV OA which is partly mediated through its neuroprotective potential linked to mitigation of tau hyperphosphorylation, apoptosis, pyroptosis, neuroinflammation, and oxidative stress and also improvement of mitochondrial health.http://www.sciencedirect.com/science/article/pii/S2405844024015950KolavironAlzheimer's diseaseCognitionApoptosisInflammationPyroptosis |
spellingShingle | Morteza Nazari-Serenjeh Tourandokht Baluchnejadmojarad Masoud Hatami-Morassa Javad Fahanik-Babaei Soraya Mehrabi Mahsa Tashakori-Miyanroudi Samira Ramazi Seyed-Mahdi Mohamadi-Zarch Davood Nourabadi Mehrdad Roghani Kolaviron neuroprotective effect against okadaic acid-provoked cognitive impairment Heliyon Kolaviron Alzheimer's disease Cognition Apoptosis Inflammation Pyroptosis |
title | Kolaviron neuroprotective effect against okadaic acid-provoked cognitive impairment |
title_full | Kolaviron neuroprotective effect against okadaic acid-provoked cognitive impairment |
title_fullStr | Kolaviron neuroprotective effect against okadaic acid-provoked cognitive impairment |
title_full_unstemmed | Kolaviron neuroprotective effect against okadaic acid-provoked cognitive impairment |
title_short | Kolaviron neuroprotective effect against okadaic acid-provoked cognitive impairment |
title_sort | kolaviron neuroprotective effect against okadaic acid provoked cognitive impairment |
topic | Kolaviron Alzheimer's disease Cognition Apoptosis Inflammation Pyroptosis |
url | http://www.sciencedirect.com/science/article/pii/S2405844024015950 |
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