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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(I_(50));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I_(50)分别为34.66、23.20、18.87μmol/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。
Objective: To investigate the effect and mechanism of honokiol on the growth of gallbladder carcinoma cells in vitro. Methods: The inhibitory effect of honokiol on SGC-996 cells was determined by CCK-8 assay and the half inhibitory concentration (I 50) was calculated. SGC-996 cells were treated with different concentrations of honokiol for 48 h After that, clone formation assay, flow cytometry and Western blot were used to detect cell clone formation, apoptosis and cell cycle, as well as apoptosis and cell cycle related protein expression. RESULTS: Honokiol significantly inhibited the growth of SGC-996 cells. The I_ (50) at 24 h, 48 h and 72 h were 34.66, 23.20 and 18.87 μmol / L, respectively. After treated with honokiol, the number of clonal cells decreased, the percentage of apoptotic cells and the percentage of cells in G0 / G1 phase increased, and the expressions of Bax, cleaved-caspase-9 and cleaved-caspase- cleaved-PARP, and decreased the expressions of Bcl-2, Bcl-2 / Bax and cyclin D1 (Cdk4, Cdk6) P <0.05). CONCLUSION: Honokiol can significantly inhibit gallbladder carcinoma cells in vitro. The mechanism may be that it induces apoptosis through initiating the intrinsic pathway of apoptosis, and inhibits the proliferation of cells by regulating the expression of cell cycle related proteins.