| Hepatic fibrosis is a compensatory response secondary to various inflammations and the liver tissue repair after injury. The activated hepatic stellate cells produce large quantities of extracellular matrix (ECM) and the extracellular matrix in liver degradation reduced . Intrahepatic extracellular matrix excessive deposition is the pathological features of hepatic fibrosis. If not be diagnosed and treatmented in time hepatic fibrosis may progress to cirrhosis and portal hypertension, which has seriously affected the physical and mental of patients. Inhibiting the activation of HSCs, and promote apoptosis in rat hepatic stellate cells is the key to the treatment of hepatic fibrosis. Inhibit the formation of collagen and accelerate the degradation of extracellular matrix is important. But the activation mechanism of hepatic stellate cells is not entirely clear.The research works about hepatic stellate cells mainly concentrated in the effect of drugs , these research works does not take into account the physical impacts in the process liver fibrosis on hepatic stellate cells . In this paper, we have done a more comprehensive analysis of the hemodynamic changes in process of liver fibrosis. We have studied the response of hepatic stellate cells to pressure in this paper. After loading intermittent pressure,typeâ… procollagen and TGF-β1 we have detected .In normal liver, hepatic stellate cells (HSCs) are nonparenchymal, quiescent cells whose main functions are to store vitamin A and probably to maintain the normal basement membrane-type matrix. HSC, which account for approximately 15% of all liver cells However, numerous in vivo and in vitro studies indicate that in response to liver injury, HSCs undergo an "activation" process in which they lose vitamin A, become highly proliferative, and synthesize "fibrotic" matrix rich in type I collagen. In liver fibrosis, intrahepatic resistance and splanchnic blood flow are increased. Inflammation, hepatic sinusoid capillarization, portal hypertension are very important factors in the hemodynamics of liver. In order to study the influence of hemodynamic factors on HSCs during hepatic fibrosis. We simulated pressure environment of the hepatic stellate cells in vitro. To investigate the effect of change in the liver sinusoids blood pressure on hepatic stellate cells. We constructed an intermittent pressure-loading (IPL) instrument.Four grades of pressure were loaded onto the hepatic stellate cells intermittently. The concentration of TGF-β1 and collagen- I in the supernatant, the amount of the protein and its mRNA in the Hepatic stellate cells were studied, respectively.We assay the effect of intermittent pressure on rat hepatic stellate cells. The growing curves of HSCs had been drawn by MTT assay. The expressions of TGF-β1 and collagen type I mRNA were detected by means of reverse transcription-polymerase chain reaction (RT-PCR). Collagen- I and TGF-β1 in the supernatants was determined by enzyme-linked immunosorbent assay (ELISA).This study concludes that intermittent pressure-loading increases transforming growth factor-beta-1 and typeâ… collagen secretion from hepatic stellate cells. These findings demonstrated that intrahepatic enhancing blood pressure might be promote hepatic fibrosis . |