Abstract
Objective To study the mechanisms involved in the regulation of endogenous β-glucuronidase expression and to explore the more effective methods to prevent recurrence of hepatolithiasis formation. Methods The expression levels of c-myc and endogenous β-glucuronidase in the liver specimens of hepatolithiasis were examined by immunohistochemical staining. The expressions of c-myc and endogenous β-glucuronidase in the human intrahepatic biliary epithelial cell line (HiBEpiC), and normal liver cell line (L02) treated with different concentrations of lipopolysaccharide (LPS) were studied using western blot. The c-myc siRNA transfection was utilized to detect the role of c-myc in the regulation of the expression of endogenous β-glucuronidase. Results Compared with normal liver samples, the expressions of endogenous β-glucuronidase and c-myc in the liver specimens of hepatolithiasis were significantly increased, and they were positively correlated with each other. LPS induced increased expressions of endogenous β-glucuronidase and c-myc in a dose-dependent manner. C-myc siRNA transfection effectively inhibited the increased expression of endogenous β-glucuronidase as induced by LPS. Conclusion LPS played a crucial role in the formation of hepatolithiasis by stimulating the endogenous expression of β-glucuronidase in liver and biliary epithelial cells via c-myc. Key words: Hepatolithiasis; β-glucuronidase; C-myc; Lipopolysaccharide (LPS)
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