Effect Of SB203580 On Apoptosis And Expression Of BCL-2 Protein In Rat Hepatic Stellate Cells

Background and aim: Liver fibrosis is due to extracellular matrix deposition in the liver over and the central of many Chronic liver disease developing to Cirrhosis. The activation of Hepatic stellate cells is the core element of liver fibrosis. Inducing apoptosis of Hepatic stellate cells can reverse the development of liver fibrosis, which is the one of important direction of treating liver fibrosis. P38MAPK is the important member of MAPK family , involving in a variety of cell activation, proliferation and apoptosis. At present the mechanisms of P38MAPK signaling pathway in hepatic stellate cells is rarely reported. To offer theoretical and experimental basis for the clinical treatment of liver fibrosis, This experiment investigate the effect of SB203580 on apoptosis of HSC-T6; the change of P-P38 protein and BCL-2 protein in HSC-T6.Methods: different concentrations of SB203580 pretreat HSC-T6 induced by acetaldehyde.The apoptosis level of HSC-T6 is detect by ELISA.The apoptosis rate of HSC-T6 is analyzed by FCM.The P-P38 protein change of HSC-T6 is observed by Western blot. The protein expression of BCL-2 is examined by SABC.Results: 1. ELSA shows that SB203580 can stimulate apoptosis of HSC-T6 induced by acetaldehyde,its increase matching with increase of SB203580 concentration(P<0.01).2. FCM shows that the apoptosis rate of HSC-T6 gradually increases with increase of SB203580 concentration(P<0.01).3. The phosphorylation of P38 protein levels is inhibited by SB203580 in a dose dependent manner (P<0.01).4. SB20380 can induce reduction protein expression of BCL-2 with apoptosis of HSC-T6.Conclusion: SB203580 can stimulate apoptosis of HSC-T6 induced by acetaldehyde, which may be related to increased levels of P38MAPK phosphorylation and inhibition of BCL-2 protein.