Hepato-gastroenterology · 2010
Protective effects of ursodeoxycholic acid against immune-mediated liver fibrosis in rats.
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Zhang Li-Xin, Liang Tie-Jun, Tan Yan-Rong, Ren Wan-Hua, Han Guo-Qing, Zhang Jie, Wang Lai-Cheng, Qin Cheng-Yong
Аннотация
BACKGROUND/AIMS: Ursodeoxycholic acid (UDCA), a natural component of bile, has been synthesized to treat cholestatic liver diseases such as primary biliary cirrhosis. Broad biochemical changes in UDCA-treated patients suggest beneficial effects of UDCA beyond stimulating hepatobiliary secretion and possible efficacy of the medicine in treating cirrhosis of other causes. The aim was to explore the potential benefit of UDCA in controlling immune-mediated hepatic fibrosis.
METHODOLOGY: We applied the rat experimental model of liver fibrosis induced by intraperitoneal injection of porcine serum. UDCA was administered orally during the course of the serum injections.
RESULTS: Compared with the untreated group, the rats treated with UDCA ended with significantly higher body weight, lower liver weight, and lower spleen weight. The treated groups also demonstrated less severe liver fibrosis, with significantly lowered hepatic expression of type I and type III collagens, in terms of both mRNA and proteins. Moreover, serum levels of hyaluronic acid (HA), laminin (LN), type IV collagen (C IV), and type III procollagen (PC III) were also lower in the UDCA-treated animals.
CONCLUSION: UDCA deters development of immune-mediated liver fibrosis by inhibiting the expression of collagen and other extracelluar matrix components.
METHODOLOGY: We applied the rat experimental model of liver fibrosis induced by intraperitoneal injection of porcine serum. UDCA was administered orally during the course of the serum injections.
RESULTS: Compared with the untreated group, the rats treated with UDCA ended with significantly higher body weight, lower liver weight, and lower spleen weight. The treated groups also demonstrated less severe liver fibrosis, with significantly lowered hepatic expression of type I and type III collagens, in terms of both mRNA and proteins. Moreover, serum levels of hyaluronic acid (HA), laminin (LN), type IV collagen (C IV), and type III procollagen (PC III) were also lower in the UDCA-treated animals.
CONCLUSION: UDCA deters development of immune-mediated liver fibrosis by inhibiting the expression of collagen and other extracelluar matrix components.