Detection Of The Bioactive Components In Herbs From Yigankang Decoction And Their Effects On TGF-β1 Downstream Signaling In Hepatic Stellate Cells

Hepatic fibrosis (HF) is a kind of chronic disease with the characteristics of excessive extra cellular matrix (ECM) deposition throughout the liver, however, without the formation of pseudo-lobules. Now it is widely accepted that HF is the inevitable and preexisting stage for lots of chronic hepatic disease developing into liver cirrhosis (LC) eventually. The pathogenesis of HF is the disequilibrium between synthesis and decomposition of ECM, resulting in large quantity of ECM depositing in the liver. The activation and proliferation of hepatic stellate cells (HSCs) play a key role in the pathogenesis of HF. Many kinds of cytokines, such as transforming growth factor β1 (TGF-β1), platelet derived growth factor (PDGF) and tumor necrosis factor a (TNF-a), were released when livers were injured by various factors. HSCs were activated by such cytokines above, then the phenotype changed from quiescent HSCs to activated myofibroblastic like cells (MFLCs), with the increasing ability of collagen production to the extent of 4-7 times compared with the quiescent cells. Therefore, abundant of extra ECM which could not be decomposed deposited in the liver, which is the key step for fibrogenesis. Accordingly, to inhibit the activation and proliferation of HSCs, promote the apoptosis of MFLCs, and decompose the collagens might be the most effective strategy to treat HF.Two kinds of cytokines—PDGF and TGF-β1, played an important role in the proliferation and phenotype transition of HSCs, respectively. TGF-β1 is the most potent cytokine of fibrogenesis known up to now, at the same time, PDGF is the factor which exerts the strongest effect on the proliferation of HSCs. More cytokines promoting fibrogenesis were released by autocrine when HSCs were activated to be MFLCs. Thus the proliferation and activation...