General overview: Neuroinflammation plays an important role in Alzheimer's disease (AD) pathogenesis. Prolonged activation of microglia can contribute to excessive production of pro-inflammatory cytokines. Neuronal stem cells (NSCs), is a potential AD therapy due to its regenerative abilities. Therefore, this study aims to investigate the regulatory effect of NSCs in lipopolysaccharides (LPS)-stimulated BV2 microglia cells. Methods: The effect of NE4C neuronal stem cell on LPS-stimulated BV2 cells were examined using transwell co-culture system. Real time reverse transcription polymerase chain reaction (qRT-PCR) and western blotting were used to study the regulation of inflammasome receptors expression that regulates the pro-inflammatory protein productions. The tested samples were further investigated for the inhibition of caspase-1 and pro-inflammatory cytokine, interleukin 1β (IL-1β) by testing the supernatants in the co-culture using caspase-1 colorimetric assay and enzyme-linked immunosorbent assay (ELISA) respectively. Results: Transwell co-culture of LPS-stimulated BV2 cells with NE4C significantly downregulated (p<0.01) mRNA expression of inflammasome receptors. Further studies on inflammasome dependent caspase-1 expression and IL-1β secretion showed NE4C inhibited inflammasome-mediated inflammation by regulating pro-inflammatory cytokines involved in activation of inflammation. Conclusion: The NE4C inhibits LPS induced neuroinflammation in BV2 cells by suppressing caspase-1 expression and IL-1β secretion through regulation of inflammasome activation.