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Tetrahydroxy stilbene glucoside ameliorates H(2)O(2)-induced human brain microvascular endothelial cell dysfunction in vitro by inhibiting oxidative stress and inflammatory responses

Tetrahydroxy stilbene glucoside (TSG) is one of the main active ingredients of Polygonum multiflorum and performs various types of biological activity, particularly anti-inflammatory and anti-oxidative activities. However, the beneficial effect of TSG in H(2)O(2)-induced human brain microvascular en...

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Autores principales: Jiang, Zhao, Wang, Wenhong, Guo, Chengcheng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5647076/
https://www.ncbi.nlm.nih.gov/pubmed/28849141
http://dx.doi.org/10.3892/mmr.2017.7225
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author Jiang, Zhao
Wang, Wenhong
Guo, Chengcheng
author_facet Jiang, Zhao
Wang, Wenhong
Guo, Chengcheng
author_sort Jiang, Zhao
collection PubMed
description Tetrahydroxy stilbene glucoside (TSG) is one of the main active ingredients of Polygonum multiflorum and performs various types of biological activity, particularly anti-inflammatory and anti-oxidative activities. However, the beneficial effect of TSG in H(2)O(2)-induced human brain microvascular endothelial cell (HBMEC) dysfunction has not been fully elucidated. In the present study, H(2)O(2)-induced oxidative stress and inflammatory responses, and the pharmacological effect of TSG were investigated. The results demonstrated that H(2)O(2) appeared to exert a cytotoxic effect on HBMECs, as the cell viability was significantly inhibited in H(2)O(2)-treated HBMECs. Conversely, TSG did not exert a toxic effect on HBMECs, and TSG inhibited H(2)O(2)-induced HBMEC cytotoxicity in a dose-dependent manner. Furthermore, the findings indicated that TSG restricted the oxidative stress caused by H(2)O(2) via inhibition of malondialdehyde and reactive oxygen species, and upregulation of superoxide dismutase and glutathione. H(2)O(2)-induced injury was associated with enhancing the levels of inflammatory cytokines, tumor necrosis factor-α, interleukin (IL)-6 and IL-1β in the cultured HBMECs, which were attenuated by TSG treatment. Furthermore, the findings demonstrated that TSG inhibited necrosis factor-κB protein expression levels, which, as an upstream transcription factor, may regulate inflammatory responses. Thus, TSG protected HBMECs from H(2)O(2)-induced dysfunction by inhibiting oxidative stress and inflammatory responses.
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spelling pubmed-56470762017-10-24 Tetrahydroxy stilbene glucoside ameliorates H(2)O(2)-induced human brain microvascular endothelial cell dysfunction in vitro by inhibiting oxidative stress and inflammatory responses Jiang, Zhao Wang, Wenhong Guo, Chengcheng Mol Med Rep Articles Tetrahydroxy stilbene glucoside (TSG) is one of the main active ingredients of Polygonum multiflorum and performs various types of biological activity, particularly anti-inflammatory and anti-oxidative activities. However, the beneficial effect of TSG in H(2)O(2)-induced human brain microvascular endothelial cell (HBMEC) dysfunction has not been fully elucidated. In the present study, H(2)O(2)-induced oxidative stress and inflammatory responses, and the pharmacological effect of TSG were investigated. The results demonstrated that H(2)O(2) appeared to exert a cytotoxic effect on HBMECs, as the cell viability was significantly inhibited in H(2)O(2)-treated HBMECs. Conversely, TSG did not exert a toxic effect on HBMECs, and TSG inhibited H(2)O(2)-induced HBMEC cytotoxicity in a dose-dependent manner. Furthermore, the findings indicated that TSG restricted the oxidative stress caused by H(2)O(2) via inhibition of malondialdehyde and reactive oxygen species, and upregulation of superoxide dismutase and glutathione. H(2)O(2)-induced injury was associated with enhancing the levels of inflammatory cytokines, tumor necrosis factor-α, interleukin (IL)-6 and IL-1β in the cultured HBMECs, which were attenuated by TSG treatment. Furthermore, the findings demonstrated that TSG inhibited necrosis factor-κB protein expression levels, which, as an upstream transcription factor, may regulate inflammatory responses. Thus, TSG protected HBMECs from H(2)O(2)-induced dysfunction by inhibiting oxidative stress and inflammatory responses. D.A. Spandidos 2017-10 2017-08-10 /pmc/articles/PMC5647076/ /pubmed/28849141 http://dx.doi.org/10.3892/mmr.2017.7225 Text en Copyright: © Jiang et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Jiang, Zhao
Wang, Wenhong
Guo, Chengcheng
Tetrahydroxy stilbene glucoside ameliorates H(2)O(2)-induced human brain microvascular endothelial cell dysfunction in vitro by inhibiting oxidative stress and inflammatory responses
title Tetrahydroxy stilbene glucoside ameliorates H(2)O(2)-induced human brain microvascular endothelial cell dysfunction in vitro by inhibiting oxidative stress and inflammatory responses
title_full Tetrahydroxy stilbene glucoside ameliorates H(2)O(2)-induced human brain microvascular endothelial cell dysfunction in vitro by inhibiting oxidative stress and inflammatory responses
title_fullStr Tetrahydroxy stilbene glucoside ameliorates H(2)O(2)-induced human brain microvascular endothelial cell dysfunction in vitro by inhibiting oxidative stress and inflammatory responses
title_full_unstemmed Tetrahydroxy stilbene glucoside ameliorates H(2)O(2)-induced human brain microvascular endothelial cell dysfunction in vitro by inhibiting oxidative stress and inflammatory responses
title_short Tetrahydroxy stilbene glucoside ameliorates H(2)O(2)-induced human brain microvascular endothelial cell dysfunction in vitro by inhibiting oxidative stress and inflammatory responses
title_sort tetrahydroxy stilbene glucoside ameliorates h(2)o(2)-induced human brain microvascular endothelial cell dysfunction in vitro by inhibiting oxidative stress and inflammatory responses
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5647076/
https://www.ncbi.nlm.nih.gov/pubmed/28849141
http://dx.doi.org/10.3892/mmr.2017.7225
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