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Resveratrol affects the migration and apoptosis of monocytes by blocking HMGB1/NF-κB pathway

BACKGROUND: Chronic inflammation is now recognized as a causal factor of aging. Resveratrol is a non-flavonoid compound that widely exists in plant species, exerting anti-inflammatory effects in vitro and in animal models. The chemotaxis of inflammatory cells and secretion of cytokines are key chara...

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Autores principales: Zhang, Yuwei, Dong, Qiaoliang, Liu, Chan, Zhu, Yingfei, Qin, Xueli, Qi, Zihan, Zhang, Xi, Guo, Hongmei, Li, Weixiang, Liu, Meng, Gan, Lin, Liu, Hong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: AME Publishing Company 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8797930/
https://www.ncbi.nlm.nih.gov/pubmed/35116666
http://dx.doi.org/10.21037/tcr-21-517
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author Zhang, Yuwei
Dong, Qiaoliang
Liu, Chan
Zhu, Yingfei
Qin, Xueli
Qi, Zihan
Zhang, Xi
Guo, Hongmei
Li, Weixiang
Liu, Meng
Gan, Lin
Liu, Hong
author_facet Zhang, Yuwei
Dong, Qiaoliang
Liu, Chan
Zhu, Yingfei
Qin, Xueli
Qi, Zihan
Zhang, Xi
Guo, Hongmei
Li, Weixiang
Liu, Meng
Gan, Lin
Liu, Hong
author_sort Zhang, Yuwei
collection PubMed
description BACKGROUND: Chronic inflammation is now recognized as a causal factor of aging. Resveratrol is a non-flavonoid compound that widely exists in plant species, exerting anti-inflammatory effects in vitro and in animal models. The chemotaxis of inflammatory cells and secretion of cytokines are key characters in inflammation response. METHODS: The effects of lipopolysaccharide (LPS) and high mobility group box-1 (HMGB1) chromosomal on the migration, inflammatory response, and apoptosis of monocytes were detected. THP-1 cells were used to study the effects of resveratrol treatment on LPS- and HMGB-induced monocytes. We aimed to investigate the effect of Resveratrol on monocyte migration and the expression of a special cytokine named HMGB1 in THP-1 cells. RESULTS: Resveratrol obviously inhibited THP-1 migration induced by LPS. LPS increased the expression of HMGB1 and its release in THP-1 cells, which were both decreased by resveratrol. Resveratrol inhibited the activity of NF-κB-p65 and the translocation of NF-κB-p65 from nucleus to cytoplasm induced by LPS. In addition, Resveratrol increased LPS and HMGB1-inhibited monocyte apoptosis. Resveratrol inhibited the LPS-induced HMGB1 secretion and its activation through NF-κB pathway. The THP-1 migration induced by LPS was inhibited by resveratrol. CONCLUSIONS: Resveratrol may inhibit monocyte migration and induce apoptosis by blocking downstream HMGB1/NF-κB/MCP-1 signaling pathways, thereby reducing systemic inflammation.
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spelling pubmed-87979302022-02-02 Resveratrol affects the migration and apoptosis of monocytes by blocking HMGB1/NF-κB pathway Zhang, Yuwei Dong, Qiaoliang Liu, Chan Zhu, Yingfei Qin, Xueli Qi, Zihan Zhang, Xi Guo, Hongmei Li, Weixiang Liu, Meng Gan, Lin Liu, Hong Transl Cancer Res Original Article BACKGROUND: Chronic inflammation is now recognized as a causal factor of aging. Resveratrol is a non-flavonoid compound that widely exists in plant species, exerting anti-inflammatory effects in vitro and in animal models. The chemotaxis of inflammatory cells and secretion of cytokines are key characters in inflammation response. METHODS: The effects of lipopolysaccharide (LPS) and high mobility group box-1 (HMGB1) chromosomal on the migration, inflammatory response, and apoptosis of monocytes were detected. THP-1 cells were used to study the effects of resveratrol treatment on LPS- and HMGB-induced monocytes. We aimed to investigate the effect of Resveratrol on monocyte migration and the expression of a special cytokine named HMGB1 in THP-1 cells. RESULTS: Resveratrol obviously inhibited THP-1 migration induced by LPS. LPS increased the expression of HMGB1 and its release in THP-1 cells, which were both decreased by resveratrol. Resveratrol inhibited the activity of NF-κB-p65 and the translocation of NF-κB-p65 from nucleus to cytoplasm induced by LPS. In addition, Resveratrol increased LPS and HMGB1-inhibited monocyte apoptosis. Resveratrol inhibited the LPS-induced HMGB1 secretion and its activation through NF-κB pathway. The THP-1 migration induced by LPS was inhibited by resveratrol. CONCLUSIONS: Resveratrol may inhibit monocyte migration and induce apoptosis by blocking downstream HMGB1/NF-κB/MCP-1 signaling pathways, thereby reducing systemic inflammation. AME Publishing Company 2021-08 /pmc/articles/PMC8797930/ /pubmed/35116666 http://dx.doi.org/10.21037/tcr-21-517 Text en 2021 Translational Cancer Research. All rights reserved. https://creativecommons.org/licenses/by-nc-nd/4.0/Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.
spellingShingle Original Article
Zhang, Yuwei
Dong, Qiaoliang
Liu, Chan
Zhu, Yingfei
Qin, Xueli
Qi, Zihan
Zhang, Xi
Guo, Hongmei
Li, Weixiang
Liu, Meng
Gan, Lin
Liu, Hong
Resveratrol affects the migration and apoptosis of monocytes by blocking HMGB1/NF-κB pathway
title Resveratrol affects the migration and apoptosis of monocytes by blocking HMGB1/NF-κB pathway
title_full Resveratrol affects the migration and apoptosis of monocytes by blocking HMGB1/NF-κB pathway
title_fullStr Resveratrol affects the migration and apoptosis of monocytes by blocking HMGB1/NF-κB pathway
title_full_unstemmed Resveratrol affects the migration and apoptosis of monocytes by blocking HMGB1/NF-κB pathway
title_short Resveratrol affects the migration and apoptosis of monocytes by blocking HMGB1/NF-κB pathway
title_sort resveratrol affects the migration and apoptosis of monocytes by blocking hmgb1/nf-κb pathway
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8797930/
https://www.ncbi.nlm.nih.gov/pubmed/35116666
http://dx.doi.org/10.21037/tcr-21-517
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