Control of JNK for an activation of NADPH oxidase in LPS-stimulated BV2 microglia

Archives of Pharmacal Research
Jung Eun Han, Ji Woong Choi

Abstract

NADPH oxidase is a main regulator for H(2)O(2) productivity in neuroinflammatory cells, including microglia, under various CNS diseases and its activity is controlled by mitogen-activated protein kinases (MAPKs), such as extracellular signal-regulated kinase 1/2 (ERK1/2), p38 MAPK, and c-Jun N-terminal kinase (JNK). However, little is known about the link between NADPH oxidase-driven H(2)O(2) productivity and JNK in microglia. The purpose of this study is to uncover the link using lipopolysaccharide (LPS)-stimulated BV2 microglia. LPS-stimulated BV2 microglia produced H(2)O(2) that was decreased by NADPH oxidase inhibitors, including 4-(2-aminoethyl)benzenesulfonylfluoride and diphenyleneiodonium chloride. In addition, NADPH oxidase was activated in LPS-stimulated BV2 cells. These results suggest that NAPDH oxidase is a main factor for H(2)O(2) productivity in LPS-stimulated BV2 microglia. Based on a semi-quantitative PCR analysis, two of NADPH oxidase components, p47(phox) and gp91(phox), were involved in the activation of NADPH oxidase because transcriptional levels of both components were upregulated by LPS. Role of JNK in NADPH oxidase-regulated H(2)O(2) productivity was pursued using specific inhibitors, including SP600125...Continue Reading

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Citations

Apr 17, 2014·Journal of Ethnopharmacology·Yanyan YangJae Youl Cho
Feb 19, 2015·Archives of Toxicology·Yongtao ZhangFan Jiang
Oct 21, 2016·Redox Biology·Calina BetlazarGuo-Jun Liu
Jun 3, 2021·Molecules : a Journal of Synthetic Chemistry and Natural Product Chemistry·Po-Jen HsuehGeorge Hsiao
Jun 2, 2018·Biomedicine & Pharmacotherapy = Biomédecine & Pharmacothérapie·Rui-Rui DingYu Zeng

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