| Objective : Liver cirrhosis is the common result of most chronic liver diseases, which is also a cosmopolitan problem in therapy. Hypohepatia,portal hypertension and much more complications will occure in its advanced stage.It threatens the patients'lives.At present, liver transplantation is the only effective therapy,however,it can not be performed widespreadly because of the lack of liver supply, the expense for operation and drugs to resist rejection for life. Hepatic fibrosis is the pathologic foundation of liver cirrhosis, and it is reversibile in its earlier period. Therefore, the major research in recent years is aimed at the treatment of hepatic fibrosis.The essence of hepatic fibrosis is the wound healing reaction of the liver.The mechanism of hepatic fibrosis maybe: When hepatic stellate cell(HSC) is activated by the stimulation of the liver causative agents, it can secrete considerable extracellular matrix (ECM),cause the disequilibrium between matrix metalloproteinase(MMPs) and tissue inhibitors of metall- oproteinase (TIMPs),and inhibit the apoptosis of HSC. The formation, development and turnover of hepatic fibrosis is determined by the activation of HSC, which is the criticality of hepatic fibrosis.Among the cell factors,it has been known that, transforming growth factor-β1 (TGF-β1) plays a key role in the priming, progress, even formation of liver cirrhosis. TGF-β1 can activate HSC and impel it to secrete more TGF-β1 , that makes a infernal circle between TGF-β1 and HSC. TGF-β1 can also promote the composition of ECM but inhibit its degradation, inhibit the regeneration of hepatic cells and promote its apoptosis. Furtherly,it can influence other cell factors associated with hepatic fibrosis and enzymes regulating matrix metabol- ism.Thus, it plays a role of causing hepatic fibrosis. The excessive TGF-β1 producted by HSC can be neutralized by TGF-β1 antibody ,thus ,its action of causing hepatic fibrosis can be resisted. The effect of TGF-β1 in HSC, cell factor network, matrix, MMPs, TIMPs and fibrinolysin has been researched penetratively in domestic and overseas.However, because of its complexity,that how to play the positive effect of TGF-β1 but inhibit its action causing hepatic fibrosis is still a focus in the scientific research in future .This research is to investigate the effect of TGF-β1 antibody on fibrotic collagen and TIMPs in the activated HSC, to confirm the reversal effect of TGF-β1 antibody on hepatic fibrosis. It is significant to the research of the occurence ,development and clinical therapy of hepatic fibrosis .Methods : This subject made rat hepatic stellate cell ( HSC-T6) as research object . HSC-T6 was subcultured to 6 sha- dow mask, and divided to 6 groups.Normal control group, TGF-β1 (1ug/L) group , TGF-β1 antibody groups(different tite ,1:100 , 1:200 , 1:400 ,1:800) were set up .Every group was cultured 6 gabs. Cells were collected 24 hours later,total RNA of HSC was extracted ,and typeâ… collagen and TIMP-1 gene expression levels were detected by quantitative analysis of reverse transcription polymerase chain reaction (RT-PCR).Results: Typeâ… collagen gene expression level in TGF-β1 group was much higher than that in normal control group (normal control group 0.405±0.063,TGF-β1 group 0.740±0.048,P<0.01).After the interference of TGF-β1 antibody 1:100 group, typeâ… collagen gene expression level started to descend compared with that in TGF-β1 group (1:100 group 0.557±0.047,P<0.01),but it was still higher than that in normal control group(P<0.01) . After the interference of TGF-β1 antibody 1:200, 1:400,1:800 groups, typeâ… collagen gene expression levels had no significant difference compared with that in normal control group and TGF-β1 group (P>0.05);TIMP-1 gene expression level in TGF-β1 group was much higher than that in normal control group(normal control group 0.613±0.068, TGF-β1 group 0.925±0.051, P<0.01).After the interference of TGF-β1 antibody 1:100 group, TIMP-1 gene expression level started to descend compared with that in TGF-β1 group(1:100 group 0.703±0.063, P<0.01), but it was still higher than that in normal control group(P<0.01) .After the interference of TGF-β1 antibody 1:200, 1:400,1:800 groups,TIMP-1 gene expression levels had no significant difference compared with that in normal control group and TGF-β1 group (P>0.05). Conclusion: TGF-β1 could promote the gene expression of typeâ… collagen and TIMP-1, hasten the development of hepatic fibrosis . TGF-β1 antibody in a certain degree could inhibit the gene expression levels of typeâ… collagen and TIMP-1, that might resist the fibrogenesis and had some therapeutic action in the reversion of hepatic fibrosis.
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