Study Of Intervention Of Fufangbiejiaruanganfang Drug Serum On The Effect On Proliferation And Activation Of Hepatic Stellate Cell In Vitro By Transforming Growth Factor

Hepatic fibrosis is a prosthetic response to chronic liver injury, still a stage ofdevelopment of kinds of chronic hepatopathy to cirrhosis of liver . The mechanism ofhepatic fibrosis is the imbalance of synthesis and degradation of extracellular matrix (ECM)by regulation of many kinds of cells and cytokines. Recently, lots of data indicate hepatocyte stellate cells (HSC) is the key cell offormation of ECM and HSC is also the core link of occurrenc of hepatic fibrosis. Variouskinds of facts lead to damage of liver, then cause Cellular necrosis of liver andinflammation. Cells which correlated hepatic fibrosis secrete cytokines to activate HSC todevelop mass of ECM, and result in a phenomenon that synthesis of ECM is more thandegradation of ECM .Kinds of cytokines regulate activation of HSC. Among thesecytokines, Platelet derived growth factor (PDGF), insulin-like growth factor-I IGF-I ,transforming growth factor TGF-β are key cytokines. There are five Isoforms TGF-β 1~5express in vertebrate,and TGF-β 1~3express inhuman and mammal. TGF-β is major cytokine which can urge HSC converse tomyofibroblasts(MFB) and excrete collagen fibers.Among these,the ratio of TGF-β 1insomatic cell is highest( 90%) and the activity of TGF-β 1is most powerful. TGF-β 1havedouble actions to HSC. TGF-β 1can induce apoptosis of HSC by influencing transcriptionfactor AP1 regulated by Smads signal pathway,or by stabilizing I B and reducing activityof NF- B. TGF-β 1can regulate genes correlated to fibrosis such as col1 1 gene, TIMPgene, PDGF gene, CTGF gene, -SMA gene and MMP-1 gene and so on to acceleratedevelopment of hepatic fibrosis.The action of TGF-β 1 to urge HSC activated is morethan which of TGF-β 1 to promote apoptosis of HSC.So the comprehensive effect of TGF-β 1is facilitate hepatic fibrosis. At present lots of study indicate tradition medicine on hepatic fibrosis have betterclinical effect and lower ill effect.Our study investigate the mechanism of treatment ofhepatic fibrosis by fufangbiejiaruanganfang. The content of fufangbiejiaruanganfanginclude biejia; dangseng; et al. We stimulate HSC sufficient activation by adding TGF-β 1to cell culture system to know the influence of fufangbiejiaruanganfang on proliferation ofHSC; activation of HSC; synthesis and degradation of extracellular matrix.英文摘要 5 1.the study of effect on secretion of TGF-β 1 in activated HSC byfufangbiejiaruanganfang drug serum In view of in vitro our experiment observe the effect on secretion of TGF-β 1 inactivated HSC by fufangbiejiaruanganfang drug serum by immunohistochemistry andimage analysis method. Our experiment indicate that IFN-γ drug serum andfufangbiejiaruanganfang drug serum decrease the secretion of TGF-β 1 from HSC.Thestrength of effect of IFN-γ drug serum is equal to low dosage fufangbiejiaruanganfangdrug serum. 2.the study of intervention of fufangbiejiaruanganfang drug serum on the effecton proliferation of HSC by TGF-β 1 Proliferation is one of key features of activation of HSC.Our experiment observe theeffect on proliferation of HSC by TGF-β 1and different serum by MTT reduction assayand flow cytometer. The result indicate that TGF-β 1, IFN-γ drug serum andfufangbiejiaruanganfang drug serum all can block cell cycle of HSC in G0G1 phase indifferent level. TGF-β 1 also can facilitate apoptosis of HSC significantly.Some studyshow that TGF-β 1 can facilitate proliferation of HSC by Smads signal pathway. Ourfinding indicates that TGF-β 1 can restrain cell cycle of HSC and facilitate apoptosis ofHSC at least in 72 hours.We conclude that TGF-β 1 may oppose or block Smads signalpathway by others signal pathway (such as NF- B signal pathway) at least in 72 hours.Sothe comprehensive effect...