PURPOSE: This study investigated the effects of an antioxidant, dihydrolipoyl histidinate zinc complex (DHLHZn), on the hepatic fibrosis in the carbon tetrachloride (CCl4) rat model. METHODS: The animals were divided into three groups: control, CCl4, and CCl4+DHLHZn. A histological assessment of the liver fibrosis was performed using stained liver samples. The oxidative stress and antioxidant levels were evaluated by measuring the malondialdehyde (MDA) and glutathione (GSH) levels in the liver. In addition, cultured human hepatic stellate cells (LI90) were exposed to antimycin-A (AMA) and divided into four groups: control, DHLHZn, AMA, and AMA+DHLHZn. The effects of DHLHZn on AMA-induced fibrosis were evaluated by measuring the expression of transforming growth factor (TGF)-β1 and collagen α1 (I). RESULTS: The hepatic fibrosis in the CCl4+DHLHZn group was attenuated compared to that in the CCl4 group. The MDA levels in the CCl4+DHLHZn group were significantly lower than those of the CCl4 group, whereas the GSH levels in the CCl4+DHLHZn group were significantly higher than those of the CCl4 group. Furthermore, the relative mRNA expression of TGF-β1 and collagen α1 (I) in the AMA+DHLHZn group was significantly lower than that in the AMA group. CONCLUSION: DHLHZn may attenuate the hepatic fibrosis induced by CCl4 by decreasing the degree of oxidative stress.
PURPOSE: This study investigated the effects of an antioxidant, dihydrolipoyl histidinate zinc complex (DHLHZn), on the hepatic fibrosis in the carbon tetrachloride (CCl4) rat model. METHODS: The animals were divided into three groups: control, CCl4, and CCl4+DHLHZn. A histological assessment of the liver fibrosis was performed using stained liver samples. The oxidative stress and antioxidant levels were evaluated by measuring the malondialdehyde (MDA) and glutathione (GSH) levels in the liver. In addition, cultured human hepatic stellate cells (LI90) were exposed to antimycin-A (AMA) and divided into four groups: control, DHLHZn, AMA, and AMA+DHLHZn. The effects of DHLHZn on AMA-induced fibrosis were evaluated by measuring the expression of transforming growth factor (TGF)-β1 and collagen α1 (I). RESULTS: The hepatic fibrosis in the CCl4+DHLHZn group was attenuated compared to that in the CCl4 group. The MDA levels in the CCl4+DHLHZn group were significantly lower than those of the CCl4 group, whereas the GSH levels in the CCl4+DHLHZn group were significantly higher than those of the CCl4 group. Furthermore, the relative mRNA expression of TGF-β1 and collagen α1 (I) in the AMA+DHLHZn group was significantly lower than that in the AMA group. CONCLUSION:DHLHZn may attenuate the hepatic fibrosis induced by CCl4 by decreasing the degree of oxidative stress.
Authors: G Svegliati Baroni; L D'Ambrosio; G Ferretti; A Casini; A Di Sario; R Salzano; F Ridolfi; S Saccomanno; A M Jezequel; A Benedetti Journal: Hepatology Date: 1998-03 Impact factor: 17.425