For example, it can regulate CRS-induced intestinal flora disorders and intestinal permeability, thereby reducing systemic LPS levels and the relative levels of AST and ALP, inhibiting the activation of the TLR4/MYD88/NF-κB signaling pathway by LPS, thereby reducing neuroinflammatory damage, and ultimately improving the depressive symptoms of CRS mice. This evidence concerns the gene NFKB1 and congenital rubella syndrome.