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Chymase converts angiotensin (Ang) I to Ang II, which may promote the development of liver fibrosis. In this study, a chymase inhibitor TY-51469 attenuated dimethylnitrosamine (DMN)-induced liver fibrosis was examined. A total of 44 rats were randomly divided into three groups: The model group, the control group, and the chymase inhibitor treatment (Chy-I) group. The rats were given intraperitoneal injections of 1% DMN (1 ml/mg). On the first day after the DMN challenge, the rats in the Chy-I group was given chymase inhibitor (10 mg/kg) by gastric lavage daily for 42 days; the other groups were given sterile saline. Liver tissue samples were collected on days 14, 28 and 56. The chymase levels were determined by enzyme-linked immunosorbent assay (ELISA). Collagen type I (Col-I) expression was evaluated by reverse-transcription polymerase chain reaction (RT-PCR). The Col-I in sinusoidal walls were evidently inhibited after the chymase inhibitor treatment, and they were higher in the liver fibrosis model group than in the control group, and significantly lower in the chymase inhibitor group. The chymase levels in the liver were evidently inhibited after the chymase inhibitor treatment, and were higher in the liver fibrosis model group than in the control group. Chymase expression was significantly lower in the Chy-I group. The Col-I mRNA levels were evidently inhibited after the chymase inhibitor treatment, higher in the liver fibrosis model group than in the control group, and significantly lower in the Chy-I group. Chymase inhibitors alleviate DMN-induced liver fibrosis in rats by inhibiting chymase activity and Col-I mRNA expression in liver tissues.       Key words: Liver fibrosis, chymase, angiotensin II, collagen type I.

Effect of chymase inhibitors on dimethylnitrosamine-induced rat liver fibrosis and on chymase and collagen I expression