金丝桃苷诱导人胃癌细胞MKN-45凋亡及其机制

Hyperoside Induces Apoptosis of Gastric Cancer Cell Line MKN-45 and Related Mechanism

目的探讨金丝桃苷(hyperoside,Hyp)对人胃癌MKN-45细胞增殖及凋亡的影响及其机制。方法体外培养MKN-45细胞,对照组不加药物,实验组分别加入不同浓度Hyp(12.5、25、50、100、200μg/ml)作用24、48 h,MTT法检测Hyp对细胞增殖的影响并筛选适宜药物浓度;流式细胞术检测细胞周期变化及凋亡率;Western blot法分析NF-κB P65、caspase-3、Bax、Bcl-2蛋白的表达情况。结果 Hyp可明显抑制MKN-45细胞的增殖,阻滞细胞于G0/G1期并促进其凋亡,Western blot结果显示,随着药物浓度的增高,Hyp可使NF-κB P65、Bcl-2蛋白表达降低,casepase-3、Bax蛋白表达增高。结论金丝桃苷可抑制MKN-45细胞增殖并诱导凋亡,其机制可能与该药物阻断细胞周期,抑制NF-κB通路,下调NF-κB P65、Bcl-2蛋白,上调casepase-3、Bax蛋白有关。

Objective To investigate the effects of hyperoside（Hyp） on the proliferation and apoptosis of human gastric cell line MKN-45 and its mechanism. Methods Gastric cells MKN-45 cultured in vitro were treated with various concentrations of hyperoside（0, 12.5, 25, 50, 100, 2009g/ml） for 24 and 48h. Cell proliferation was examined by MTT which could screen suitable drug concentration; cell cycle and apoptosis were analyzed by flow cytometry; NF-κB P65, casepase-3, Bcl-2 and Bax protein expressions were examined by Western blot. Results Hyperoside could inhibit the growth of MKN-45 cells observably, it also blocked cell cycle at G0/G1 stage and induced cell apoptosis. Western blot showed that hyperoside could reduce the expression of NF-κB P65, Bcl-2 protein and elevate the expression of caspase-3, Bax protein with the increase of drug concentration. Conclusion Hyperoside could inhibit the growth of MKN-45 cells and induce cell apoptosis. The mechanism might be related to blocking cell cycle, inhibiting NF-κB pathway, reducing the expression of NF-κB P65 and Bcl-2 protein and elevating the expression of caspase-3 and Bax protein.