Furthermore, in vitro experiments confirmed that the acetate and butyrate-key metabolites of B. coprocola-attenuated the inflammatory responses and promoted M2-like macrophage polarization via free fatty acid receptor (FFAR) 2/3 receptors, thereby suppressing NLRP3 activation.<h4>Conclusions</h4>In conclusion, B. coprocola treatment can improve motor deficits, neuroinflammation, and intestinal function in the rotenone-induced PD mouse model. The gene discussed is NLRP3; the disease is Parkinson disease.