ABSTRACT
OBJECTIVE： To observe the improvement effect and mechanism of 4-hydroxy-2-benzoxazolone （HBOA） on carbon tetrachloride-induced hepatic fibrosis in rats. METHODS： Male SD rats were randomly divided into normal control group， model group， colchicine group （positive control， 0.4 mg/kg） and HBOA low-dose， medium-dose and high-dose groups （50， 75， 100 mg/kg）， with 12 rats in each group. Except for normal control group was given constant volume of normal saline intragastrically， other groups were given 50％CCl4-olive oil solution （2 mL/kg， initial dose double） intragastrically， twice a week， for consecutive 12 weeks， to induce hepatic fibrosis model. Since the 9th week of modeling， administration groups were given relevant medicine intragastrically. Normal control group and model group were given constant volume of 0.6％ Carboxymethylcellulose sodium solution intragastrically， once a day， for consecutive 4 weeks. After last administration， the serum contents of ALT， AST， IL-1β and IL-10， the protein expression of NF-κB p65， TNF-α， IL-6 and ICAM-1 in liver tissue were determined. RESULTS： Compared with normal control group， the positive expression of NF-κB p65 in liver tissue was increased significantly in model group； serum contents of ALT， AST and IL-1β as well as protein expression of NF-κB p65， TNF-α， IL-6 and ICAM-1 in liver tissure were increased significantly， while serum content of IL-10 was decreased significantly （P＜0.05）. Compared with model group， the positive expression of NF-κB p65 in liver tissue were decreased to different extents in administration groups； serum contents of ALT， AST and IL-1β as well as protein expression of NF-κB p65， TNF-α， IL-6 and ICAM-1 in liver tissue were decreased significantly， while serum content of IL-10 was increased significantly （P＜0.05）. CONCLUSIONS： HBOA can improve carbon tetrachloride-induced hepatic fibrosis in rats， and the mechanism of which may be associated with relieving inflammatory reaction by blocking NF-κB signaling pathway and down-regulating the protein expression of ICAM-1.