This improvement was accompanied by the suppression of M1 cytokine expression, such as IL-6, TNF-α, and inducible nitric oxide synthase (iNOS), while supporting the transcription of M2 cytokines (Arg-1 and IL-10) in lipopolysaccharide (LPS)-challenged mouse microglia, an shifting microglia from pro-inflammatory CD86 (M1 markers) to anti-inflammatory CD206 (M2 marker) in the early stage of post-stroke neuroinflammation [41]. Here, TNF is linked to stroke disorder.