Hepatic
fibrosis is an important pathological manifestation of chronic schistosome
infection. Patients with advanced
schistosomiasis show varying degrees of abnormalities in
liver fibrosis indicators and
bilirubin metabolism. However, the relationship between hepatic
fibrosis in
schistosomiasis and dysregulated
bilirubin metabolism remains unclear. In this study, we observed a positive correlation between total
bilirubin levels and the levels of ALT, AST, LN, and CIV in patients with advanced
schistosomiasis. Additionally, we established mouse models at different time points following S. japonicum
infection. As the
infection time increased,
liver fibrosis escalated, while liver UGT1A1 consistently exhibited a low expression, indicating impaired glucuronidation of
bilirubin metabolism in mice. In vitro experiments suggested that SEA may be a key inhibitor of hepatic UGT1A1 expression after schistosome
infection. Furthermore, a high concentration of
bilirubin activated the NF-κB signaling pathway in L-O2 cells in vitro. These findings suggested that the dysregulated glucuronidation of
bilirubin caused by S. japonicum
infection may play a significant role in
schistosomiasis liver fibrosis through the NF-κB signaling pathway.