The Study of the Neuroprotective Effect of the Extract from <i>Chelidonium Majus</i> L. <i>in Vitro</i>

The protection of neurons from damage and death is an important challenge in the development of treatment of brain ischemia and neurodegenerative diseases. This study aims to investigate protective effect of the extract prepared from Chelidonium majus, which contains total alkaloids. In the present...

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Autores principales: A. Zhalsrai, L. Ts. Sanzhieva
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Lenguaje:RU
Publicado: Scientific Сentre for Family Health and Human Reproduction Problems 2019
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Acceso en línea:https://doaj.org/article/5d1e5b194c4b40898571d40cc47f794b
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spelling oai:doaj.org-article:5d1e5b194c4b40898571d40cc47f794b2021-11-23T06:14:42ZThe Study of the Neuroprotective Effect of the Extract from <i>Chelidonium Majus</i> L. <i>in Vitro</i>2541-94202587-959610.29413/ABS.2019-4.2.15https://doaj.org/article/5d1e5b194c4b40898571d40cc47f794b2019-05-01T00:00:00Zhttps://www.actabiomedica.ru/jour/article/view/2053https://doaj.org/toc/2541-9420https://doaj.org/toc/2587-9596The protection of neurons from damage and death is an important challenge in the development of treatment of brain ischemia and neurodegenerative diseases. This study aims to investigate protective effect of the extract prepared from Chelidonium majus, which contains total alkaloids. In the present study, we examined antioxidant activity of total alkaloids from Chelidonium majus in vitro. Hydroxyl radical and lipid radicals were detected using spin trapping agents with ESR spectrometer. Chelidonium majus extract exhibited dose-dependent scavenging effects on lipid radicals. Halfmaximal inhibitory concentration (IC50) of the extract was 2.96 mg/ml, whereas for hydroxyl radicals it was 55.13 mg/ ml. These results showed that extract of Chelidonium majus is partly inhibited free radicals. Antioxidant effects of this extract were further demonstrated by protecting enzyme activity of the mitochondrial respiratory electron transport chain (complex I) in isolated brain mitochondrial dysfunction induced by MDA. However, it did not change the decreased level of complex II, and malate dehydrogenase (MDH) in a concentration of 12 and 25 mg/ml. Here, we examined the neuroprotective effect of the extract from Chelidonium majus against oxidative stress in cultured cortical neurons, using MTT. We found that pretreatment with the extract of Chelidonium majus (0.05 and 0.5 mg/ml) significantly inhibited H2O2-induced cell death in cortical neurons.Furthermore, the use of a luciferase reporter (ARE-luc) assay showed that extract from Chelidonium majus activates protective signaling pathway in primary cortical neurons through ARE/Nrf2 pathway.Together, this suggests that total alkaloids from Chelidonium majus may be neuroprotective by increasing anti-oxidant gene expression.A. ZhalsraiL. Ts. SanzhievaScientific Сentre for Family Health and Human Reproduction Problemsarticlechelidonium majus lneuroprotection effectsantioxidant responsive elementsScienceQRUActa Biomedica Scientifica, Vol 4, Iss 2, Pp 106-113 (2019)
institution DOAJ
collection DOAJ
language RU
topic chelidonium majus l
neuroprotection effects
antioxidant responsive elements
Science
Q
spellingShingle chelidonium majus l
neuroprotection effects
antioxidant responsive elements
Science
Q
A. Zhalsrai
L. Ts. Sanzhieva
The Study of the Neuroprotective Effect of the Extract from <i>Chelidonium Majus</i> L. <i>in Vitro</i>
description The protection of neurons from damage and death is an important challenge in the development of treatment of brain ischemia and neurodegenerative diseases. This study aims to investigate protective effect of the extract prepared from Chelidonium majus, which contains total alkaloids. In the present study, we examined antioxidant activity of total alkaloids from Chelidonium majus in vitro. Hydroxyl radical and lipid radicals were detected using spin trapping agents with ESR spectrometer. Chelidonium majus extract exhibited dose-dependent scavenging effects on lipid radicals. Halfmaximal inhibitory concentration (IC50) of the extract was 2.96 mg/ml, whereas for hydroxyl radicals it was 55.13 mg/ ml. These results showed that extract of Chelidonium majus is partly inhibited free radicals. Antioxidant effects of this extract were further demonstrated by protecting enzyme activity of the mitochondrial respiratory electron transport chain (complex I) in isolated brain mitochondrial dysfunction induced by MDA. However, it did not change the decreased level of complex II, and malate dehydrogenase (MDH) in a concentration of 12 and 25 mg/ml. Here, we examined the neuroprotective effect of the extract from Chelidonium majus against oxidative stress in cultured cortical neurons, using MTT. We found that pretreatment with the extract of Chelidonium majus (0.05 and 0.5 mg/ml) significantly inhibited H2O2-induced cell death in cortical neurons.Furthermore, the use of a luciferase reporter (ARE-luc) assay showed that extract from Chelidonium majus activates protective signaling pathway in primary cortical neurons through ARE/Nrf2 pathway.Together, this suggests that total alkaloids from Chelidonium majus may be neuroprotective by increasing anti-oxidant gene expression.
format article
author A. Zhalsrai
L. Ts. Sanzhieva
author_facet A. Zhalsrai
L. Ts. Sanzhieva
author_sort A. Zhalsrai
title The Study of the Neuroprotective Effect of the Extract from <i>Chelidonium Majus</i> L. <i>in Vitro</i>
title_short The Study of the Neuroprotective Effect of the Extract from <i>Chelidonium Majus</i> L. <i>in Vitro</i>
title_full The Study of the Neuroprotective Effect of the Extract from <i>Chelidonium Majus</i> L. <i>in Vitro</i>
title_fullStr The Study of the Neuroprotective Effect of the Extract from <i>Chelidonium Majus</i> L. <i>in Vitro</i>
title_full_unstemmed The Study of the Neuroprotective Effect of the Extract from <i>Chelidonium Majus</i> L. <i>in Vitro</i>
title_sort study of the neuroprotective effect of the extract from <i>chelidonium majus</i> l. <i>in vitro</i>
publisher Scientific Сentre for Family Health and Human Reproduction Problems
publishDate 2019
url https://doaj.org/article/5d1e5b194c4b40898571d40cc47f794b
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