| Hepatic fibrosis represents a wound-healing process in response to a variety of chronic live injury. Hepatic fibrosis is associated with major alterations in both the quantity and composition of ECM (extracellular matrix). The histological change of hepatic fibrosis is characterized by an excessive deposition of extracellular matrix proteins of which type I collagen predominates. The excess deposition of ECM disrupts the normal architecture of the liver leading to the organ failure.Hepatic stellate cells (HSCs) have been considered as the main ECM-producing cells during hepatic fibrosis, and HSCs are observed with a dramatic increase in proliferation and type I collagen synthesis. It is believed that effective treatment regimes aimed at reducing the synthesis of ECM or proliferation of HCSs would reduce the progression of fibrosis. The activation of HSCs is the key issue in the pathogenesis of hepatic fibrosis, which is mediated by various cytokines. Platelet-derived growth factor (PDGF) is the most potent proliferative cytokine for the HSCs. Whether PDGF increases the synthesis of type I collagen of HCSc as well as increases the proliferation of HSCs is still controversial. PDGF has been shown to transmit proliferative signals through phosphatidylionsitol 3-kinase (PI3K) pathway in several cell types, but there are few reports in HSCs. More researchers are paying close attention to signaling pathway to understand the mechanism of hepatic fibrosis. The author sought to investigate the effects of PDGF and the role of PI3K pathway in hepatic fibrosis, to explore the therapeutics for hepatic fibrosis.Part IObjective: To investigate the effects of PDGF-BB in rat HSCs proliferation and type I collagen synthesis.Methods: Rat HSCs were stimulated by different concentrations of PDGF-BB. Cell proliferation was assessed by MTT colorimetric assay. Flow cytometric analysis was carried out to cell cycle.The type I collagen protein was assayed by ELISA. The mRNA of...
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