NADPH oxidase is a main regulator for $H_2O_2$ 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 oxidasedriven $H_2O_2$ 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 $H_2O_2$ 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 $H_2O_2$ 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 $H_2O_2$ productivity was pursued using specific inhibitors, including SP600125 and JNK inhibitory peptide (JIP). Inhibition of the JNK pathways significantly reduced $H_2O_2$ productivity, which was closely related to the attenuation of NADPH oxidase activation and the upregulation of components. We conclude that JNK pathways are involved in NADPH oxidase-mediated $H_2O_2$ productivity in BV2 microglia.