AIM:To explore the role of focal adhesion kinase(FAK)in the apoptosis in culture-activated rat hepatic stellatecells(HSCs)using a specific anti-FAK antibody.METHODS:Rat HSCs were prepared from Wistar rats byin situ perfusion of collagenase and pronase and single-step density Nycodenze gradient.Culture-activatedHSCs were serum-starved and treated with the anti-FAK antibodies for 24,48 or 72 h.The apoptosis of HSCwas detected by DNA-fragment assay,flow cytometryand caspase-3 activity determination.The expressionof tissue inhibitor of metalloproteinase-1(TIMP-1)mRNA was assessed by reverse transcriptionpolymerase chain reaction(RT-PCR).RESULTS:The experiment showed that anti-FAKantibodies induced apoptosis of culture-activated ratHSCs.This phenomenon displayed the classical featuresof apoptotic cell death(DNA fragmentation,cell cycleanalysis)after treated with 30 mg·L~(-1)FAK antibody for72 h,and accompanied by a significant increase ofcaspase-3 activity(1208±76)vs(309±28)nmol·min~(-1)·g~(-1),t=208.5,P<0.05.Meanwhile,treatment with theFAK antibody in HSCs could markedly decrease theTIMP-1 mRNA expression(0.07±0.01 vs0.38±0.03,t=2.72,P<0.05).CONCLUSION:FAK plays an important role in the survivalof HSCs and the specific anti-FAK antibody could inducethe apoptosis in rat HSCs. AIM: To explore the role of focal adhesion kinase (FAK) in the apoptosis in culture-activated rat hepatic stellate cells (HSCs) using a specific anti-FAK antibody. METHODS: Rat HSCs were prepared from Wistar rats by in situ perfusion of collagenase and pronase and single-step density Nycodenze gradient. Culture-activated HSCs were serum-starved and treated with the anti-FAK antibodies for 24, 48 or 72 h. The apoptosis of HSC was detected by DNA-fragment assay, flow cytometry and caspase-3 activity determination. The expression of tissue inhibitor of metalloproteinase-1 (TIMP-1) mRNA was assessed by reverse transcription polymerase chain reaction (RT-PCR) .RESULTS: The experiment showed that anti-FAKantibodies induced apoptosis of culture-activated rat HSCs.This phenomenon displayed the classical features of apoptotic cell death (DNA fragmentation, cell cycle analysis) after treated with 30 mg · L -1 FAK antibody for 72 h, accompanied by a significant increase of caspase-3 activity (1208 ± 76) vs (309 ± 28) nmol · min ~ (-1 ) · G ~ (-1), t = 208.5, P <0.05. Meanwhile, treatment with the FAK antibody in HSCs could markedly decrease the TIMP-1 mRNA expression (0.07 ± 0.01 vs 0.38 ± 0.03, t = ). CONCLUSION: FAK plays an important role in the survival of HSCs and the specific anti-FAK antibody could induce the apoptosis in rat HSCs.