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http://dx.doi.org/10.15324/kjcls.2020.52.3.253

Metformin or α-Lipoic Acid Attenuate Inflammatory Response and NLRP3 Inflammasome in BV-2 Microglial Cells  

Choi, Hye-Rim (Department of Biomedical Laboratory Science, Konyang University)
Ha, Ji Sun (Department of Biomedical Laboratory Science, Konyang University)
Kim, In Sik (Department of Biomedical Laboratory Science, School of Medicine, Eulji University)
Yang, Seung-Ju (Department of Biomedical Laboratory Science, Konyang University)
Publication Information
Korean Journal of Clinical Laboratory Science / v.52, no.3, 2020 , pp. 253-260 More about this Journal
Abstract
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-inflammatory 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.
Keywords
${\alpha}$-lipoic acid; Amyloid beta; Metformin; NLRP3 inflammasome; S100A9;
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Times Cited By KSCI : 5  (Citation Analysis)
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