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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 combination 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 t 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 vs0.210±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 vs0 .l00±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 in group I tended to decrease (0.449±0.028 vs0.513±0.016,P＜0.05).CONCLUSION: PDGF may promote proliferation of HSCsbut is neutral with respect to HSC apoptosis. TL-10 may promote the 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.