<i>Thunbergia laurifolia</i> Leaf Extract Inhibits Glutamate-Induced Neurotoxicity and Cell Death through Mitophagy Signaling

Oxidative stress plays a crucial role in neurodegeneration. Therefore, reducing oxidative stress in the brain is an important strategy to prevent neurodegenerative disorders. <i>Thunbergia laurifolia</i> (Rang-jued) is well known as an herbal tea in Thailand. Here, we aimed to determine...

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Autores principales: Wudtipong Vongthip, Chanin Sillapachaiyaporn, Kyu-Won Kim, Monruedee Sukprasansap, Tewin Tencomnao
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Publicado: MDPI AG 2021
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Acceso en línea:https://doaj.org/article/cab76b1d7dfc4e4380d0989ec6242811
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spelling oai:doaj.org-article:cab76b1d7dfc4e4380d0989ec62428112021-11-25T16:25:55Z<i>Thunbergia laurifolia</i> Leaf Extract Inhibits Glutamate-Induced Neurotoxicity and Cell Death through Mitophagy Signaling10.3390/antiox101116782076-3921https://doaj.org/article/cab76b1d7dfc4e4380d0989ec62428112021-10-01T00:00:00Zhttps://www.mdpi.com/2076-3921/10/11/1678https://doaj.org/toc/2076-3921Oxidative stress plays a crucial role in neurodegeneration. Therefore, reducing oxidative stress in the brain is an important strategy to prevent neurodegenerative disorders. <i>Thunbergia laurifolia</i> (Rang-jued) is well known as an herbal tea in Thailand. Here, we aimed to determine the protective effects of <i>T. laurifolia</i> leaf extract (TLE) on glutamate-induced oxidative stress toxicity and mitophagy-mediated cell death in mouse hippocampal cells (HT-22). Our results reveal that TLE possesses a high level of bioactive antioxidants by LC–MS technique. We found that the pre-treatment of cells with TLE prevented glutamate-induced neuronal death in a concentration-dependent manner. TLE reduced the intracellular ROS and maintained the mitochondrial membrane potential caused by glutamate. Moreover, TLE upregulated the gene expression of antioxidant enzymes (SOD1, SOD2, CAT, and GPx). Interestingly, glutamate also induced the activation of the mitophagy process. However, TLE could reverse this activity by inhibiting autophagic protein (LC3B-II/LC3B-I) activation and increasing a specific mitochondrial protein (TOM20). Our results suggest that excessive glutamate can cause neuronal death through mitophagy-mediated cell death signaling in HT-22 cells. Our findings indicate that TLE protects cells from neuronal death by stimulating the endogenous antioxidant enzymes and inhibiting glutamate-induced oxidative toxicity via the mitophagy–autophagy pathway. TLE might have potential as an alternative or therapeutic approach in neurodegenerative diseases.Wudtipong VongthipChanin SillapachaiyapornKyu-Won KimMonruedee SukprasansapTewin TencomnaoMDPI AGarticleautophagyglutamatemitophagyneurodegenerative diseasesoxidative stress<i>Thunbergia laurifolia</i>Therapeutics. PharmacologyRM1-950ENAntioxidants, Vol 10, Iss 1678, p 1678 (2021)
institution DOAJ
collection DOAJ
language EN
topic autophagy
glutamate
mitophagy
neurodegenerative diseases
oxidative stress
<i>Thunbergia laurifolia</i>
Therapeutics. Pharmacology
RM1-950
spellingShingle autophagy
glutamate
mitophagy
neurodegenerative diseases
oxidative stress
<i>Thunbergia laurifolia</i>
Therapeutics. Pharmacology
RM1-950
Wudtipong Vongthip
Chanin Sillapachaiyaporn
Kyu-Won Kim
Monruedee Sukprasansap
Tewin Tencomnao
<i>Thunbergia laurifolia</i> Leaf Extract Inhibits Glutamate-Induced Neurotoxicity and Cell Death through Mitophagy Signaling
description Oxidative stress plays a crucial role in neurodegeneration. Therefore, reducing oxidative stress in the brain is an important strategy to prevent neurodegenerative disorders. <i>Thunbergia laurifolia</i> (Rang-jued) is well known as an herbal tea in Thailand. Here, we aimed to determine the protective effects of <i>T. laurifolia</i> leaf extract (TLE) on glutamate-induced oxidative stress toxicity and mitophagy-mediated cell death in mouse hippocampal cells (HT-22). Our results reveal that TLE possesses a high level of bioactive antioxidants by LC–MS technique. We found that the pre-treatment of cells with TLE prevented glutamate-induced neuronal death in a concentration-dependent manner. TLE reduced the intracellular ROS and maintained the mitochondrial membrane potential caused by glutamate. Moreover, TLE upregulated the gene expression of antioxidant enzymes (SOD1, SOD2, CAT, and GPx). Interestingly, glutamate also induced the activation of the mitophagy process. However, TLE could reverse this activity by inhibiting autophagic protein (LC3B-II/LC3B-I) activation and increasing a specific mitochondrial protein (TOM20). Our results suggest that excessive glutamate can cause neuronal death through mitophagy-mediated cell death signaling in HT-22 cells. Our findings indicate that TLE protects cells from neuronal death by stimulating the endogenous antioxidant enzymes and inhibiting glutamate-induced oxidative toxicity via the mitophagy–autophagy pathway. TLE might have potential as an alternative or therapeutic approach in neurodegenerative diseases.
format article
author Wudtipong Vongthip
Chanin Sillapachaiyaporn
Kyu-Won Kim
Monruedee Sukprasansap
Tewin Tencomnao
author_facet Wudtipong Vongthip
Chanin Sillapachaiyaporn
Kyu-Won Kim
Monruedee Sukprasansap
Tewin Tencomnao
author_sort Wudtipong Vongthip
title <i>Thunbergia laurifolia</i> Leaf Extract Inhibits Glutamate-Induced Neurotoxicity and Cell Death through Mitophagy Signaling
title_short <i>Thunbergia laurifolia</i> Leaf Extract Inhibits Glutamate-Induced Neurotoxicity and Cell Death through Mitophagy Signaling
title_full <i>Thunbergia laurifolia</i> Leaf Extract Inhibits Glutamate-Induced Neurotoxicity and Cell Death through Mitophagy Signaling
title_fullStr <i>Thunbergia laurifolia</i> Leaf Extract Inhibits Glutamate-Induced Neurotoxicity and Cell Death through Mitophagy Signaling
title_full_unstemmed <i>Thunbergia laurifolia</i> Leaf Extract Inhibits Glutamate-Induced Neurotoxicity and Cell Death through Mitophagy Signaling
title_sort <i>thunbergia laurifolia</i> leaf extract inhibits glutamate-induced neurotoxicity and cell death through mitophagy signaling
publisher MDPI AG
publishDate 2021
url https://doaj.org/article/cab76b1d7dfc4e4380d0989ec6242811
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