<i>Chrysanthemum indicum</i> Prevents Hydrogen Peroxide-Induced Neurotoxicity by Activating the TrkB/Akt Signaling Pathway in Hippocampal Neuronal Cells

Oxidative stress-mediated neuronal damage is associated with the pathogenesis and development of neurodegenerative diseases. <i>Chrysanthemum indicum</i> has antioxidant properties. However, the neuroprotective effects and the cellular mechanism of <i>C. indicum</i> ethanol e...

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Autores principales: Yun Hee Jeong, Tae In Kim, You-Chang Oh, Jin Yeul Ma
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Publicado: MDPI AG 2021
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spelling oai:doaj.org-article:e03f10563ec74182a6d8341213cd90af2021-11-25T18:33:13Z<i>Chrysanthemum indicum</i> Prevents Hydrogen Peroxide-Induced Neurotoxicity by Activating the TrkB/Akt Signaling Pathway in Hippocampal Neuronal Cells10.3390/nu131136902072-6643https://doaj.org/article/e03f10563ec74182a6d8341213cd90af2021-10-01T00:00:00Zhttps://www.mdpi.com/2072-6643/13/11/3690https://doaj.org/toc/2072-6643Oxidative stress-mediated neuronal damage is associated with the pathogenesis and development of neurodegenerative diseases. <i>Chrysanthemum indicum</i> has antioxidant properties. However, the neuroprotective effects and the cellular mechanism of <i>C. indicum</i> ethanol extract (CIE) against oxidative damage in hippocampal neuronal cells have not been clearly elucidated. Therefore, this study investigated whether CIE has protective effects against hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>)-induced oxidative toxicity in HT22 cells. CIE pretreatment significantly improved neuronal cell viability. Moreover, the formation of intracellular reactive oxygen species and apoptotic bodies, and mitochondrial depolarization were significantly reduced in HT22 cells with H<sub>2</sub>O<sub>2</sub>-induced oxidative toxicity. Furthermore, CIE increased the phosphorylation of tropomyosin-related kinase receptor B (TrkB), protein kinase B (Akt), cAMP response element-binding protein, the expression of brain-derived neurotrophic factor, antioxidant enzymes, and the nuclear translocation of nuclear factor erythroid 2-related factor 2 by activating the TrkB/Akt signaling pathway. In contrast, the addition of K252a, a TrkB inhibitor, or MK-2206, an Akt-selective inhibitor, reduced the neuroprotective and antioxidant effects of CIE. Taken together; CIE exhibits neuroprotective and antioxidant effects against oxidative damage. Therefore, it can be a potential agent for treating oxidative stress-related neurodegenerative diseases.Yun Hee JeongTae In KimYou-Chang OhJin Yeul MaMDPI AGarticle<i>Chrysanthemum indicum</i>neuroprotective effectsantioxidantnuclear factor erythroid 2-related factor 2tropomyosin-related kinase receptor Bprotein kinase BNutrition. Foods and food supplyTX341-641ENNutrients, Vol 13, Iss 3690, p 3690 (2021)
institution DOAJ
collection DOAJ
language EN
topic <i>Chrysanthemum indicum</i>
neuroprotective effects
antioxidant
nuclear factor erythroid 2-related factor 2
tropomyosin-related kinase receptor B
protein kinase B
Nutrition. Foods and food supply
TX341-641
spellingShingle <i>Chrysanthemum indicum</i>
neuroprotective effects
antioxidant
nuclear factor erythroid 2-related factor 2
tropomyosin-related kinase receptor B
protein kinase B
Nutrition. Foods and food supply
TX341-641
Yun Hee Jeong
Tae In Kim
You-Chang Oh
Jin Yeul Ma
<i>Chrysanthemum indicum</i> Prevents Hydrogen Peroxide-Induced Neurotoxicity by Activating the TrkB/Akt Signaling Pathway in Hippocampal Neuronal Cells
description Oxidative stress-mediated neuronal damage is associated with the pathogenesis and development of neurodegenerative diseases. <i>Chrysanthemum indicum</i> has antioxidant properties. However, the neuroprotective effects and the cellular mechanism of <i>C. indicum</i> ethanol extract (CIE) against oxidative damage in hippocampal neuronal cells have not been clearly elucidated. Therefore, this study investigated whether CIE has protective effects against hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>)-induced oxidative toxicity in HT22 cells. CIE pretreatment significantly improved neuronal cell viability. Moreover, the formation of intracellular reactive oxygen species and apoptotic bodies, and mitochondrial depolarization were significantly reduced in HT22 cells with H<sub>2</sub>O<sub>2</sub>-induced oxidative toxicity. Furthermore, CIE increased the phosphorylation of tropomyosin-related kinase receptor B (TrkB), protein kinase B (Akt), cAMP response element-binding protein, the expression of brain-derived neurotrophic factor, antioxidant enzymes, and the nuclear translocation of nuclear factor erythroid 2-related factor 2 by activating the TrkB/Akt signaling pathway. In contrast, the addition of K252a, a TrkB inhibitor, or MK-2206, an Akt-selective inhibitor, reduced the neuroprotective and antioxidant effects of CIE. Taken together; CIE exhibits neuroprotective and antioxidant effects against oxidative damage. Therefore, it can be a potential agent for treating oxidative stress-related neurodegenerative diseases.
format article
author Yun Hee Jeong
Tae In Kim
You-Chang Oh
Jin Yeul Ma
author_facet Yun Hee Jeong
Tae In Kim
You-Chang Oh
Jin Yeul Ma
author_sort Yun Hee Jeong
title <i>Chrysanthemum indicum</i> Prevents Hydrogen Peroxide-Induced Neurotoxicity by Activating the TrkB/Akt Signaling Pathway in Hippocampal Neuronal Cells
title_short <i>Chrysanthemum indicum</i> Prevents Hydrogen Peroxide-Induced Neurotoxicity by Activating the TrkB/Akt Signaling Pathway in Hippocampal Neuronal Cells
title_full <i>Chrysanthemum indicum</i> Prevents Hydrogen Peroxide-Induced Neurotoxicity by Activating the TrkB/Akt Signaling Pathway in Hippocampal Neuronal Cells
title_fullStr <i>Chrysanthemum indicum</i> Prevents Hydrogen Peroxide-Induced Neurotoxicity by Activating the TrkB/Akt Signaling Pathway in Hippocampal Neuronal Cells
title_full_unstemmed <i>Chrysanthemum indicum</i> Prevents Hydrogen Peroxide-Induced Neurotoxicity by Activating the TrkB/Akt Signaling Pathway in Hippocampal Neuronal Cells
title_sort <i>chrysanthemum indicum</i> prevents hydrogen peroxide-induced neurotoxicity by activating the trkb/akt signaling pathway in hippocampal neuronal cells
publisher MDPI AG
publishDate 2021
url https://doaj.org/article/e03f10563ec74182a6d8341213cd90af
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