Metformin or α-Lipoic Acid Attenuate Inflammatory Response and NLRP3 Inflammasome in BV-2 Microglial Cells
Alzheimer’s disease (AD) is a chronic and progressive neurodegenerative disease that can be described by the occurrence of dementia due to a decline in cognitive function. The disease is characterized by the formation of extracellular and intracellular amyloid plaques. Amyloid beta (Aβ) is a hallmar...
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doaj-110e08104258465c80388c0f2f0439812020-11-25T01:23:05ZengThe Korean Society for Clinical Laboratory ScienceKorean Journal of Clinical Laboratory Science1738-35442288-16622020-09-0152325326010.15324/kjcls.2020.52.3.253Metformin or α-Lipoic Acid Attenuate Inflammatory Response and NLRP3 Inflammasome in BV-2 Microglial CellsHye-Rim Choi0Ji Sun Ha1In Sik Kim2Seung-Ju Yang3https://orcid.org/0000-0001-9261-2749Department of Biomedical Laboratory Science, Konyang University, Daejeon, Korea Department of Biomedical Laboratory Science, Konyang University, Daejeon, Korea Department of Biomedical Laboratory Science, School of Medicine, Eulji University, Daejeon, KoreaDepartment of Biomedical Laboratory Science, Konyang University, Daejeon, Korea Alzheimer’s disease (AD) is a chronic and progressive neurodegenerative disease that can be described by the occurrence of dementia due to a decline in cognitive function. The disease is characterized by the formation of extracellular and intracellular amyloid plaques. Amyloid beta (Aβ) is a hallmark of AD, and microglia can be activated in the presence of Aβ. Activated microglia secrete pro-inflammatory cytokines. Furthermore, S100A9 is an important innate immunity pro-inflam-matory contributor in inflammation and a potential contributor to AD. This study examined the effects of metformin and α-LA on the inflammatory response and NLRP3 inflammasome activation in Aβ- and S100A9-induced BV-2 microglial cells. Metformin and α-LA attenuated inflammatory cytokines, such as tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6). In addition, metformin and α-LA inhibited the phosphorylation of JNK, ERK, and p38. They activated the nuclear factor kappa B (NF-κB) pathway and the NOD-like receptor pyrin domain containing 3 (NLRP3) inflammasome. Moreover, metformin and α-LA reduced the marker levels of the M1 phenotype, ICAM1, whereas the M2 phenotype, ARG1, was increased. These findings suggest that metformin and α-LA are therapeutic agents against the Aβ- and S100A9-induced neuroinflammatory responses.α-lipoic acidamyloid betametforminnlrp3 inflammasomes100a9 |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Hye-Rim Choi Ji Sun Ha In Sik Kim Seung-Ju Yang |
spellingShingle |
Hye-Rim Choi Ji Sun Ha In Sik Kim Seung-Ju Yang Metformin or α-Lipoic Acid Attenuate Inflammatory Response and NLRP3 Inflammasome in BV-2 Microglial Cells Korean Journal of Clinical Laboratory Science α-lipoic acid amyloid beta metformin nlrp3 inflammasome s100a9 |
author_facet |
Hye-Rim Choi Ji Sun Ha In Sik Kim Seung-Ju Yang |
author_sort |
Hye-Rim Choi |
title |
Metformin or α-Lipoic Acid Attenuate Inflammatory Response and NLRP3 Inflammasome in BV-2 Microglial Cells |
title_short |
Metformin or α-Lipoic Acid Attenuate Inflammatory Response and NLRP3 Inflammasome in BV-2 Microglial Cells |
title_full |
Metformin or α-Lipoic Acid Attenuate Inflammatory Response and NLRP3 Inflammasome in BV-2 Microglial Cells |
title_fullStr |
Metformin or α-Lipoic Acid Attenuate Inflammatory Response and NLRP3 Inflammasome in BV-2 Microglial Cells |
title_full_unstemmed |
Metformin or α-Lipoic Acid Attenuate Inflammatory Response and NLRP3 Inflammasome in BV-2 Microglial Cells |
title_sort |
metformin or α-lipoic acid attenuate inflammatory response and nlrp3 inflammasome in bv-2 microglial cells |
publisher |
The Korean Society for Clinical Laboratory Science |
series |
Korean Journal of Clinical Laboratory Science |
issn |
1738-3544 2288-1662 |
publishDate |
2020-09-01 |
description |
Alzheimer’s disease (AD) is a chronic and progressive neurodegenerative disease that can be described by the occurrence of dementia due to a decline in cognitive function. The disease is characterized by the formation of extracellular and intracellular amyloid plaques. Amyloid beta (Aβ) is a hallmark of AD, and microglia can be activated in the presence of Aβ. Activated microglia secrete pro-inflammatory cytokines. Furthermore, S100A9 is an important innate immunity pro-inflam-matory contributor in inflammation and a potential contributor to AD. This study examined the effects of metformin and α-LA on the inflammatory response and NLRP3 inflammasome activation in Aβ- and S100A9-induced BV-2 microglial cells. Metformin and α-LA attenuated inflammatory cytokines, such as tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6). In addition, metformin and α-LA inhibited the phosphorylation of JNK, ERK, and p38. They activated the nuclear factor kappa B (NF-κB) pathway and the NOD-like receptor pyrin domain containing 3 (NLRP3) inflammasome. Moreover, metformin and α-LA reduced the marker levels of the M1 phenotype, ICAM1, whereas the M2 phenotype, ARG1, was increased. These findings suggest that metformin and α-LA are therapeutic agents against the Aβ- and S100A9-induced neuroinflammatory responses. |
topic |
α-lipoic acid amyloid beta metformin nlrp3 inflammasome s100a9 |
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