目的：探讨和厚朴酚在体外对胆囊癌细胞生长的影响及机制。方法：用CCK-8法检测和厚朴酚对胆囊癌SGC-996细胞的抑制作用，并计算其半数抑制浓度（IC50）；用不同浓度和厚朴酚作用SGC-996细胞48 h后，分别用平板克隆形成试验、流式细胞术，Western blot法检测细胞克隆形成、凋亡与细胞周期情况，以及凋亡及细胞周期相关蛋白的表达。结果：和厚朴酚能明显抑制SGC-996细胞的生长，其24、48、72 h的IC50分别为34.66、23.20、18.87 μmol/L。和厚朴酚处理后的SGC-996细胞克隆细胞团数减少，细胞的凋亡率与G0/G1期细胞百分比增加，促凋亡蛋白（Bax、cleaved-caspase-9、cleaved-caspase-3、cleaved-PARP）表达升高、抗凋亡蛋白（Bcl-2、Bcl-2/Bax比值）与细胞周期相关蛋白（Cyclin D1、Cdk4、Cdk6）表达降低，且均呈明显的浓度依赖趋势（均P<0.05）。结论：和厚朴酚在体外对胆囊癌细胞有明显的抑制作用，其机制可能是通过启动细胞凋亡内始式途径诱导细胞凋亡，并且通过调节细胞周期相关蛋白的表达抑制细胞的增殖。
Inhibitory effect of honokiol against gallbladder cancer in vitro and its mechanism
Objective: To investigate the effect of honokiol on the growth of gallbladder cancer cells in vitro and its mechanism. Methods: Using CCK-8 assay, the inhibitory effect of honokiol on gallbladder cancer SGC-996 cells was observed and the 50% inhibitory concentration (IC50) values were calculated. After exposure of SGC-996 cells to different concentrations of honokiol for 48 h, the colony formation, apoptosis and cell cycle as well as the expressions of apoptosis and cell cycle related proteins were examined by plate colony formation assay, cytometry and Western blot analysis, respectively. Results: Honokiol significantly inhibited the growth of SGC-996 cells, and its IC50 value was 34.66, 23.20 and 18.87 μmol/L after 24, 48 and 72 h, respectively. After exposure of SGC-996 cells to honokiol, the number of colony forming units was decreased, apoptosis rate and percentage of G0/G1 cells were increased, and the expressions of pro-apoptotic proteins (Bax, cleaved-caspase-9, cleaved-caspase-3 and cleaved-PARP) were increased, while expressions of anti-apoptotic proteins (Bcl-2 and Bcl-2/Bax ratio) as well as cell cycle-related proteins (Cyclin D1, Cdk4 and Cdk6) were decreased. All of these effects showed significant concentration-dependent trend (all P<0.05). Conclusion: Honokiol has strong inhibitory effect on gallbladder cancer cells in vitro, and its mechanism may possibly be associated with inducing cell apoptosis via intrinsic apoptosis pathway and suppressing cell proliferation by regulating the expression of cell cycle-related proteins.