Neuroinflammation is involved in the pathogenesis of many neurodegenerative diseases, including Parkinson's Disease, primarily resulting from microglial activation. Microglia are the primary phagocytic cells of the central nervous system, and their activation play a significant role in neuroinflammation. Microglial activation and the changes in their morphological appearance depend on the actin cytoskeleton reorganization. WASP family Verprolin-homologous protein-2 (WAVE2), a member of Wiskott Aldrich's Syndrome Proteins, is a primary regulator of actin cytoskeleton. This study is aimed to test the effect of WAVE2 inhibition on inflammatory phenotype of BV-2 microglial cells. We have shown that lipopolysaccharides (LPS) stimulation significantly upregulates oxidative stress and nuclear factor kappa-B (NF-kB) signaling, and cause changes in appearance of BV-2 microglial cells. Knocking down WAVE2 with the help of adeno-associated virus vector does not block these outcomes. These data suggest that the inflammatory phenotype of microglial cells may not be primarily dependent on WAVE2 signaling.