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High glucose enhances lipopolysaccharide‐induced inflammation in cultured BV2 microglial cell line
INTRODUCTION: Diabetes mellitus emerges as a global health crisis and is related to the development of neurodegenerative diseases. Microglia, a population of macrophages‐like cells, govern immune defense in the central nervous system. Activated microglia are known to play active roles in the pathoge...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9017628/ https://www.ncbi.nlm.nih.gov/pubmed/35478445 http://dx.doi.org/10.1002/iid3.610 |
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author | Hung, Hao‐Chang Tsai, Sheng‐Feng Sie, Shih‐Ren Kuo, Yu‐Min |
author_facet | Hung, Hao‐Chang Tsai, Sheng‐Feng Sie, Shih‐Ren Kuo, Yu‐Min |
author_sort | Hung, Hao‐Chang |
collection | PubMed |
description | INTRODUCTION: Diabetes mellitus emerges as a global health crisis and is related to the development of neurodegenerative diseases. Microglia, a population of macrophages‐like cells, govern immune defense in the central nervous system. Activated microglia are known to play active roles in the pathogenesis of neurodegenerative diseases. METHODS: This study aimed to investigate the effects of high glucose on low‐dose lipopolysaccharide (LPS)‐induced activations of inflammation‐related signaling molecules in cultured BV2 microglial cells. RESULTS: Compared to cells cultured in the normal glucose medium (NGM, 5.5 mM), the LPS‐induced activation of NF‐κB lasted longer in cells cultured in high glucose medium (HGM, 25 mM). HGM also enhanced the expression of inducible nitric oxide synthase (iNOS). Among the mitogen‐activated protein kinases, HGM enhanced the LPS‐induced phosphorylation of p38 without affecting the phosphorylation of Erk1/2 or JNK. BV2 cells cultured in HGM expressed higher levels of TLR4 than those cells cultured in NGM. CONCLUSION: High glucose aggravated LPS‐induced inflammatory responses of microglia via enhancing the TLR4/p38 pathway and prolonging the activation of NF‐κB/iNOS signaling. Controlling blood glucose levels is advised to manage neuroinflammation and related neurodegenerative diseases. |
format | Online Article Text |
id | pubmed-9017628 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-90176282022-04-21 High glucose enhances lipopolysaccharide‐induced inflammation in cultured BV2 microglial cell line Hung, Hao‐Chang Tsai, Sheng‐Feng Sie, Shih‐Ren Kuo, Yu‐Min Immun Inflamm Dis Original Articles INTRODUCTION: Diabetes mellitus emerges as a global health crisis and is related to the development of neurodegenerative diseases. Microglia, a population of macrophages‐like cells, govern immune defense in the central nervous system. Activated microglia are known to play active roles in the pathogenesis of neurodegenerative diseases. METHODS: This study aimed to investigate the effects of high glucose on low‐dose lipopolysaccharide (LPS)‐induced activations of inflammation‐related signaling molecules in cultured BV2 microglial cells. RESULTS: Compared to cells cultured in the normal glucose medium (NGM, 5.5 mM), the LPS‐induced activation of NF‐κB lasted longer in cells cultured in high glucose medium (HGM, 25 mM). HGM also enhanced the expression of inducible nitric oxide synthase (iNOS). Among the mitogen‐activated protein kinases, HGM enhanced the LPS‐induced phosphorylation of p38 without affecting the phosphorylation of Erk1/2 or JNK. BV2 cells cultured in HGM expressed higher levels of TLR4 than those cells cultured in NGM. CONCLUSION: High glucose aggravated LPS‐induced inflammatory responses of microglia via enhancing the TLR4/p38 pathway and prolonging the activation of NF‐κB/iNOS signaling. Controlling blood glucose levels is advised to manage neuroinflammation and related neurodegenerative diseases. John Wiley and Sons Inc. 2022-04-19 /pmc/articles/PMC9017628/ /pubmed/35478445 http://dx.doi.org/10.1002/iid3.610 Text en © 2022 The Authors. Immunity, Inflammation and Disease published by John Wiley & Sons Ltd. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Articles Hung, Hao‐Chang Tsai, Sheng‐Feng Sie, Shih‐Ren Kuo, Yu‐Min High glucose enhances lipopolysaccharide‐induced inflammation in cultured BV2 microglial cell line |
title | High glucose enhances lipopolysaccharide‐induced inflammation in cultured BV2 microglial cell line |
title_full | High glucose enhances lipopolysaccharide‐induced inflammation in cultured BV2 microglial cell line |
title_fullStr | High glucose enhances lipopolysaccharide‐induced inflammation in cultured BV2 microglial cell line |
title_full_unstemmed | High glucose enhances lipopolysaccharide‐induced inflammation in cultured BV2 microglial cell line |
title_short | High glucose enhances lipopolysaccharide‐induced inflammation in cultured BV2 microglial cell line |
title_sort | high glucose enhances lipopolysaccharide‐induced inflammation in cultured bv2 microglial cell line |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9017628/ https://www.ncbi.nlm.nih.gov/pubmed/35478445 http://dx.doi.org/10.1002/iid3.610 |
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