New Insights into Baicalein’s Effect on Chlorpyrifos-Induced Liver Injury in Carp: Involving Macrophage Polarization and Pyropto sis

, is a potent anti-inflammatory, antioxidant, and antitumor agent. The objective of this paper is to investigate the molecular mechanism by which Bai prevents CPF-induced hepatotoxic injury. Carp were kept in water containing CPF (23.2 μg/L) and/or fed diets containing Bai (0.15 g/kg). We found that Bai attenuated liver tissue damage and vacuolization caused by CPF. We confirmed that CPF causes M1/M2 polarization imbalance in macrophages and hepatocyte pyroptosis, which ultimately leads to liver injury. Further exploration of the internal mechanism shows that CPF participates in liver toxicity damage by destroying the AMPK/SIRT1/pGC-1α pathway and causing mitochondrial biogenesis and mitochondrial dynamics imbalance. Notably, Bai significantly attenuated CPF-induced inhibition of the AMPK/SIRT1/pGC-1α pathway. In summary, our results suggest that Bai alleviates CPF exposure-induced inhibition of the AMPK/SIRT1/pGC-1α pathway, thereby attenuating macrophage M1 hyperpolarization and pyroptosis by inhibiting the NF-κB pathway. These results may provide new insights into the detoxification mechanism of Bai on the same type of organophosphorus pesticides.