目的　观察Sulindac对人肝癌细胞HepG2增殖、凋亡及β-catenin蛋白表达的影响，探讨Sulindac抗肝癌的可能机制。  方法　不同浓度的Sulindac作用HepG2细胞后，采用MTT实验检测细胞增殖抑制作用；采用Hoechst33258染色法检测Sulindac对HepG2细胞凋亡的影响；利用RT-PCR及Western blotting检测HepG2细胞在Sulindac作用后Wint通路中β-catenin的表达变化。 结果　Sulindac对人肝癌细胞HepG2有增殖抑制作用，且呈剂量时间依赖关系；Hoechst33258结果显示，Sulindac作用24 h后HepG2细胞凋亡数目明显增多；随着Sulindac浓度的增加，β-catenin mRNA及蛋白表达量逐渐下降。  结论　Sulindac能够抑制人肝癌细胞HepG2增殖，通过阻断Wnt信号传导通路，降低β-catenin表达，诱导人肝癌细胞HepG2的凋亡。

Objective　To observe the effect of Sulindac on proliferation, apoptosis of human liver cancer cell HepG2 and the expression of β-catenin protein, and to investigate the possible anti-cancer mechanism of Sulindac.　Methods　HepG2 cells were treated with different dose of Sulindac. The inhibitory effect of Sulindac on proliferation was detected by MTT assay. Hoechst 33258 staining was applied to analyze the effect of Sulindac on apoptosis of HepG2 cell. The expression ofβ-catenin protein in the Wnt pathway was detected by RT-PCR and Western blotting.　Results　Sulindac could inhibit the proliferation of liver cancer cell HepG2 with time and dose dependence. The number of apoptotic cells after treated with Sulindac for 24h was larger than those treated with DMSO. The expression of β-catenin appeared to decrease with the increase of drug concentration.  Conclusion　Sulindac can inhibit the growth of liver cancer HepG2 cells. It can block the Wnt signal transduction pathway, and reduce the expression ofβ-catenin, which may be the mechanism of its anti-tumor effect.