AIM:To investigate the effects of platelet-derived growthfactor(PDGF) and interleukin-10 (IL-10) on Fas/Fas-ligandand Bcl-2/Bax mRNA expressions in rat hepatic stellate cells.METHODS:Rat hepatic stellate cells (HSCs) were isolatedand purified from rat liver by in situ digestion of collagenaseand pronase and single-step density Nycodenz gradient.After activated by culture in vitro,HSCs were divided into4 groups and treated with nothing (group N),PDGF (group P),IL-10 (group I) and PDGF in cornbination with IL-10 (group C),respectively.Semi-quantitative reverse-transcriptasepolymerase chain reaction (RT-PCR) analysis was employedto compare the mRNA expression levels of Fas/FasL and Bcl-2/Bax in HSCs of each group.RESULTS:The expression levels of Fas between the 4 groupshad no significant differences (P>0.05).FasL mRNA levelin normal culture-activated HSCs (group N) was very low.It increased obviously after HSCs were treated with IL-10(group I) (0.091±0.007 vs 0.385±0.051,P<0.01),butremained the low level after treated with PDGF alone (group P)or PDGF in combination with IL-10 (group C).Contrast tothe control group,after treated with PDGF and IL-10,eitheralone or in combination,Bcl-2 mRNA expression was down-regulated and Bax mRNA expression was up-regulated,bothfollowing the turn from group P,group I to group C.Expression of Bcl-2 mRNA in group C was significantly lowerthan that in group P (0.126±0.008 vs 0.210±0.024,P<0.01).But no significant difference was found between group Cand group I,as well as between group I and group P (P>0.05).Similarly,the expression of Bax in group C was higherthan that in group P (0.513±0.016 vs 0.400±0.022,P<0.01).No significant difference was found between group I and groupP (P>0.05).But compared with group C,Bax expressions ingroup I tended to decrease (0.449±0.028 vs 0.513±0.016,P<0.05).CONCLUSION:PDGF may promote proliferation of HSCsbut is neutral with respect to HSC apoptosis.IL-10 may promotethe apoptosis of HSCs by up-regulating the expressions of FasLand Bax and down-regulating the expression of Bcl-2,whichmay be involved in its antifibrosis mechanism. AIM: To investigate the effects of platelet-derived growth factor (PDGF) and interleukin-10 (IL-10) on Fas / Fas-ligand and Bcl-2 / Bax mRNA expressions in rat hepatic stellate cells. METHODS: Rat hepatic stellate cells ) were isolated and purified from rat liver by in situ digestion of collagenase and pronase and single-step density Nycodenz gradient. After activated by culture in vitro, HSCs were divided into 4 groups and treated with nothing (group N), PDGF (group P), IL -10 (group I) and PDGF in cornbination with IL-10 (group C), respectively. Semi-quantitative reverse-transcriptase polymerase chain reaction (RT-PCR) was used to compare the mRNA expression levels of Fas / FasL and Bcl-2 / Bax in HSCs of each group .RESULTS: The expression levels of Fas between the 4 groupshad no significant differences (P> 0.05) .FasL mRNA levelin normal culture-activated HSCs (group N) was very low. It increased obviously after HSCs were treated with IL-10 (group I) (0.091 ± 0.007 vs. 0.385 ± 0.051, P <0.01), butrema ined the low level after treated with PDGF alone (group P) or PDGF in combination with IL-10 (group C). Contrast tothe control group, after treated with PDGF and IL-10, eitheralone or in combination, Bcl-2 mRNA expression was down-regulated and Bax mRNA expression was up-regulated, bothfollowing the turn from group P, group I to group C. Expression of Bcl-2 mRNA in group C was significantly lowerthan that in group P (0.126 ± 0.008 vs 0.210 ± 0.024 , P <0.01) .But no significant difference was found between group Cand group I, as well as between group I and group P (P> 0.05) .Similarly, the expression of Bax in group C was higherthan that in group P (0.513 ± 0.016 vs 0.400 ± 0.022, P <0.01) .No significant difference was found between group I and group P (P> 0.05) .But compared with group C, Bax expressions group I tended to decrease (0.449 ± 0.028 vs 0.513 ± 0.016, P <0.05) .CONCLUSION: PDGF may promote proliferation of HSCsbut is neutral with respect to HSC apoptosis. IL-10 may promotethe apoptosis of HSCs by up-reg ulatingthe expressions of FasLand Bax and down-regulating the expression of Bcl-2, whichmay be involved in its antifibrosis mechanism.