Furthermore, the most pronounced functional network overrepresented in these data involved NF-��B complex, stat1-stat2, irf1 and irf9, which form the central molecule of an interconnected regulatory system, Ropivacaine hydrochloride suggesting that NF-��B complex, stat1-stat2, irf1 and irf9 link proinflammatory cytokines to mediate the signaling and induction of proinflammatory activities in microglia in response to LPS stimulation. The up-regulation of NF-��B complex, stat1-stat2, irf1 and irf9 in LPS-stimulated BV-2 microglial cells was further illustrated in the differential gene expression analysis. In the present study, we examined BV2 cell lines as a model of inflammation studies. This is one of the major uses of microglia. Previously, others reports demonstrated that BV-2 cell lines have close resemblance to primary brain microglia. Consistent with our findings, Hennet al. reported that in the presence of LPS transcriptome and proteome analysis of BV-2 cell lines revealed a high similarity to primary microglial cells. Since BV-2cells are easy to culture, they are an important tool to study not only inflammatory processes, but also phagocytosis. Recently, reported that BV-2 cell lines exhibit many similarities to that of primary microglia and in vivo in terms of Huntington’s disease. In contrast, demonstrated that indifferent conditions, such as after exposure to macrophage colony-stimulating factor and transforming growth factor beta1 adult primary microglia showed a unique molecular expression pattern. However, MCSF and TGF-?1 did not induce such microglial molecular expression pattern in BV-2 cell lines. In the presence of LPS as well as MCSF and TGF-?1 detailed transcriptome analysis will be required to determine the unique transcriptomic signature in primary microglial cells. Overall, the genome-wide analysis through RNA-Seq showed LPS-inducible genes in microglial cells, reflecting the robust and reliable kinetic development and modulation of cell reactivity during the early course of the inflammatory response.Regardless of certain boundaries in exactitude, LPS-stimulated inflammatory gene expression profiling in microglia, clustering, and the prediction of cis-regulatory elements offer Lumiracoxib valuable information for future studies, such as potential gene targets for chromatin immunoprecipitation-seq assays.