In the PTC-209 present study, we used an RNA-Seq approach to profile the differential gene expression at multiple time-points inBV-2 microglial cells in response to inflammatory stimulus. Although other methods, such as microarray technology, have been applied for the genome-wide analysis of inflammatory gene transcription in macrophages, the experimental strategy described here provided novel insights into high-resolution transcriptome data. RNA-Seq technology, combined with bioinformatics, is an efficient high-throughput tool to establish gene expression patterns and complete functional RI-1 clustering, canonical pathway and network enrichment of DEGs, with great advantages for identifying host response genes and obtaining associated information following LPS infection. Bioinformatics analyses of DEGs revealed approximately 263 and 319 genes were significantly up-regulated after 2and 4h, respectively, in LPS-stimulated BV-2 cells. This variation between 2h and 4h time point maybe due to relatively less immune response gene expression level at its earliest stage of bacterial infection when high variation is more pronounced compared to the 4h time point. Notably, these data were accurate, although two independent biological replicates for each sample were used. In addition, we investigated the use of differential promoters, transcription start sites and isoforms variants in LPS-stimulated geneloci, which, to our knowledge, has not been previously validated in studies concerning genome-wide gene regulation in microglia. We observed that LPS significantly induced the expression of key pro-inflammatory enzymes, including nos2 and ptgs2. Nos2 plays a pivotal role in mediating neuro inflammation to produce NO, a potent proinflammatory mediator, via oxidative deamination. Because neurons and oligodendrocytes are injurious in relation to NO, an oversupply of NO can cause nerve injury in CNS diseases. Ptgs2 is the key enzyme responsible for brain inflammation, and increased ptgs2 expression contributes to neuro degeneration.Ccl12 also plays an inflammatory role, as the levels of this chemokine are up-regulated in both microglia and astrocytes when stimulated with the proinflammatory cytokine il-17