Cancer informatics · 2026
Clostridium-Derived p-Cresyl Metabolites Induce Inflammation and Apoptosis in Biliary Epithelial Cells.
СтатьяНазвание и аннотация: Перевод в очереди
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Yu Haiyan, Fu Haiyan, Xu Jiamin, Yang Yina, Ai Xin, Tu Rongfang, Bao Weimin, Tang Yingmei
Аннотация
OBJECTIVE: Primary biliary cholangitis (PBC) is an autoimmune cholestatic liver disease, and the effects of p-cresyl sulfate (PCS) and p-cresyl glucuronide (PCG) in PBC remain unclear. This study aimed to evaluate the pro-apoptotic and pro-inflammatory effects of PCS and PCG.
METHODS: Human intrahepatic biliary epithelial cells (HIBEpiCs) were treated with PCS or PCG, and apoptosis was assessed by flow cytometry. Female C57BL/6 mice received intraperitoneal PCS or PCG. Liver inflammation was evaluated by H&E staining, apoptosis-related proteins (caspase-3, Bax, Bcl-2) by Western blotting, and serum TGF-β and IFN-γ by ELISA.
RESULTS: PCS and PCG increased apoptosis in HIBEpiCs. In vivo, PCS and PCG treated mice displayed portal lymphocytic infiltration and elevated serum IFN-γ and TGF-β. Hepatic caspase-3 and Bax were upregulated, whereas Bcl-2 was downregulated in a time-dependent manner.
CONCLUSIONS: PCS and PCG promote intrahepatic inflammation and BEC apoptosis, suggesting that gut microbial metabolites may contribute to hepatobiliary immune injury.
METHODS: Human intrahepatic biliary epithelial cells (HIBEpiCs) were treated with PCS or PCG, and apoptosis was assessed by flow cytometry. Female C57BL/6 mice received intraperitoneal PCS or PCG. Liver inflammation was evaluated by H&E staining, apoptosis-related proteins (caspase-3, Bax, Bcl-2) by Western blotting, and serum TGF-β and IFN-γ by ELISA.
RESULTS: PCS and PCG increased apoptosis in HIBEpiCs. In vivo, PCS and PCG treated mice displayed portal lymphocytic infiltration and elevated serum IFN-γ and TGF-β. Hepatic caspase-3 and Bax were upregulated, whereas Bcl-2 was downregulated in a time-dependent manner.
CONCLUSIONS: PCS and PCG promote intrahepatic inflammation and BEC apoptosis, suggesting that gut microbial metabolites may contribute to hepatobiliary immune injury.