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目的 研究棕榈酸对转化生长因子β1(TGF-β1)刺激的肝星状细胞(HSC)增殖、凋亡及半胱氨酸天冬氨酸蛋白酶12(caspase-12)蛋白表达的影响.方法 将液氮保存下的肝星状细胞株,于37℃、5％ CO2孵箱中进行复苏传代培养,同步化后将细胞分为5组:空白组、TGF-β1(5 ng/ml)组、TGF-β1+低、中、高剂量棕榈酸组,即5 ng/ml TGF-β1刺激24 h,再分别加入50、100及200μmol/L不同剂量棕榈酸作用24 h后,用MTT比色法检测细胞增殖、流式细胞仪检测细胞凋亡率、免疫细胞化学法测定Caspase-12蛋白表达.结果 不同浓度棕榈酸均能抑制细胞增殖(P＜0.05),且随着剂量的增加,细胞相对增殖率(RGR)降低,低、中、高剂量组分别为76.56％、60.93％和34.37％,组间比较差异有统计学意义(P＜0.05).透视电镜发现,不同剂量棕榈酸组出现细胞核变小,细胞出现大量线粒体空泡,染色质边集等典型凋亡表现.空白组、TGF-β1组、TGF-β1+低、中、高剂量棕榈酸组凋亡率分别为(3.32±0.29)％、(1.70±0.14)％、(7.26±0.46)％、(11.24±0.52)％及(15.55±0.31)％,组间两两比较差异有统计学意义(P＜0.05);随着棕榈酸剂量的增加,细胞Caspase-12蛋白表达增加(P＜0.05).结论 棕榈酸能抑制细胞增殖,增加Caspase-12蛋白表达,促进HSC凋亡.“,”Objective To investigate the effect of palmitic acid (PA) on caspase-12 and proliferation and apoptosis in rat hepatic stellate cells (HSCs) when stimulated by transforming growth factor-β1 (TGF-β1).Methods HSCs were randomly divided into five groups:Sham group,TGF-β1 group,TGF-β1 + low PA group,TGF-β1 + middle PA group and TGF-β1 + high PA group.HSCs were stimulated by TGF-β1 (5 ng/ml) for 24 hours followed by co-incubation with PA under different doses (50,100,and 200 umol/L).No intervention was performed in Sham group.Cell proliferation was detected by MTT;morphological manifestations of cells were obtained by transmission electronmicroscope;apoptosis rate was determined by flow cytometry;expression levels of caspase-12 was measured by Immunohistochemistry.Results Cellular proliferation was significantly inhibited with PA treatment in a dose dependent manner (P ＜ 0.05).Transmission electronmicroscope showed typical apoptotic features such as small nuclei,large numbers of mitochondria vacuoles and obvious edge sets of DNA.Treatment of PA dramatically increased apoptosis rate when compared with TGF-β1 group [(7.26± 0.46)％ vs (1.70 ± 0.14) ％,P＜ 0.05;(11.24 ± 0.52) ％ vs (1.70 ± 0.14) ％,P＜ 0.05;(15.55 ± 0.31) ％ vs (1.70 ± 0.14) ％,P ＜ 0.05].Expression of caspase-12 protein increased significantly with PA in dose dependent manner (P ＜0.05).Conclusion PA inhibits cellular proliferation through promoting caspase-12 mediated apoptosis in HSCs.