Experimental Study Of GSB On Hepatic Fibrosis Caused By Paragonimus Skrjabini In Rats

【Objective】The aim of this experiment is to observe whether it is necessary to make further anti-fibrosis treatment after Triclabendazole therapy on rat liver fibrosis caused by Pagumogonimus skrjabini;observe the effects of GSB on rat liver fibrosis caused by Pagurnogonimus skrjabini;explore the mechanism of GSB's anti-fibrosis function;we provide some experimental evidence for finding a new kind of medcine that with positive curative effect,minimal side effects for treating hepatic fibrosis caused by Pagumogonimus skrjabini.【Methods】Seventy SD rats were divided into seven groups.One group was used as normal group(negative control group).Each of the other groups of rats was induced by 15 metacercariae of Pagumogonimus skrjabini after 8 weeks and made into fibrosis model.These rats were divided into:model group,triclabendazole treated group,theγ-interferon combined with triclabendazole treated group and the gentiana scabra bge combined with triclabendazole treated group(low dose,medium dose,high dose).IFN-γ,as a positive control.The rats were killed at the end of the twelfth week, the pathology of liver fibrosis was observed with HE stain and VG stain. Immunohistochemistry was used to observe the expression of collagenⅠ,Ⅲand TIMP-1 protein in liver samples.【Results】1.Triclabendazole insecticidal treatment to improve the degree of liver fibrosis was not obvious,the expression of collagenⅠ,Ⅲ,TIMP-1 protein in liver were not markedly reduced according to immunohistochemistry analysis,with no difference in model group(P＞0.05).2.Upon pathological examination,the GSB(medium dose,high dose) treatment had significantly reversed Pagumogonimus skrjabini-induced liver fibrosis.In GSB(medium dose,high dose) treatment group, the GSB could obviously improve the pathological changes in liver and enhance the degradation of collagen in the rat fibrotic liver according to HE and VG staining compared with the fibrotic model group(P＜0.05).Liver fibrosis score significantly lower(P＜0.05).Moreover,in GSB(medium dose,high dose)treatment group,the expressions of collagenⅠ,Ⅲ,TIMP-1 positive area in liver were markedly reduced, according to immunohistochemistry analysis as compared with model group.These effects were dose-dependent.But the GSB(low dose) treatment group,had no significantly reversed Pagumogonimus skrjabini-induced liver fibrosis upon pathological examination,the GSB(low dose) treatment group could not obviously improve the pathological changes in liver and enhance the degradation of collagen in the rat fibrotic liver according to HE and VG staining compared with the fibrotic model group(P＞0.05).Liver fibrosis score is no significantly lower(P＞0.05),the expression of collagenⅠ,Ⅲ,TIMP-1 positive area in liver was not obviously reduced, according to immunohistochemistry analysis as compared with model group(P＞0.05).【Conclusions】1) Anti-fibrotic treatment is necessary after the treatment of praziquantel.2) The rat hepatic fibrosis induced by Pagumogonimus skrjabini can be obviously reversed by GSB.The anti-fibrotic effect of GSB is based on reducing synthesis and enhancing degradation of collagen.GSB treatment of liver fibrosis there is a certain dose range.3) GSB may be provide a new approach for the treatment of liver fibrosis and early cirrhosis.