Compound Biejia-Ruangan tablets activate the STING-TBK1 pathway to alleviate hepatic fibrosis in alveolar echinococcosis

. CBRT suppressed the activation of HSCs, partly by upregulating IFN-γ, suppressed apoptosis in GHA1 hepatocytes, and improved hepatocyte function. Mechanistically, CBRT activates the STING-TBK1 signaling pathway, which subsequently suppresses the polarization of macrophages toward the M2 phenotype, thereby alleviating fibrogenesis. This study demonstrates that CBRT alleviates hepatic fibrosis by activating the STING-TBK1 signaling pathway. This activation elicits a shift in macrophage polarization from the pro-fibrotic M2 phenotype towards the M1 phenotype, which subsequently suppresses the activation of hepatic stellate cells and alleviates fibrogenesis. These findings reveal a novel immunomodulatory mechanism of CBRT centered on the STING-TBK1 axis, providing both experimental evidence and a theoretical foundation for its potential application in treating hepatic fibrosis associated with AE. IMPORTANCE: )-induced hepatic fibrosis by reactivating the suppressed STING-TBK1 signaling pathway in the chronic infection stage, thereby reprogramming macrophage polarization from a pro-fibrotic M2 phenotype toward an M1 phenotype. This work identifies CBRT as a promising immunomodulatory agent that can reverse the Th2/M2-dominated immunosuppressive microenvironment, providing a novel therapeutic strategy for AE and potentially other infection-associated fibrotic diseases. However, further research is required to validate the translational efficacy of CBRT and to define the precise therapeutic window for STING-TBK1 modulation in human fibrotic disorders.