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目的探讨银杏叶提取物(ginkgo biloba extract,EGb761)对顺铂诱导的胃癌细胞SGC-7901及胃癌耐药细胞SGC-7901/CDDP增殖和凋亡的影响及其对胃癌细胞化疗耐药的影响及其机制。方法采用EGb761、顺铂单用及EGb761与顺铂联合应用处理人胃癌细胞株SGC-7901及耐药细胞SGC-7901/CDDP,采用四甲基偶氮唑蓝(methyl thiazolyl tetrazolium,MTT)法检测两种细胞的增殖活性,流式细胞仪检测细胞凋亡,实时荧光定量PCR法、Western blot法检测两种细胞中NIBP、NF-κB P65 mR NA和蛋白的表达。结果顺铂和EGb761均对两种胃癌细胞的增殖具有抑制作用,呈剂量依赖性,但SGC-7901/CDDP细胞对顺铂的敏感性较SGC-7901/CDDP差。EGb761与顺铂联合应用可明显增强SGC-7901及SGC-7901/CDDP细胞株对顺铂的敏感性并促进细胞的凋亡。SGC-7901/CDDP细胞中NIBP和NF-κB p65的mR NA及蛋白相对表达水平均高于SGC-7901细胞(P<0.05),EGb761能明显抑制由顺铂诱导的NIBP和NF-κB p65的表达(P<0.05)。结论 EGb761具有显著的化疗增敏效果,并能逆转胃癌细胞耐药,增强顺铂对胃癌细胞生长的抑制作用并促进细胞凋亡。其逆转抗肿瘤细胞耐药和化疗增敏的作用机制可能是通过抑制NF-κB通路的活性,减少NIBP和NF-κB p65的表达而实现。
Objective To investigate the effect of ginkgo biloba extract (EGb761) on proliferation and apoptosis of gastric cancer cell line SGC-7901 and gastric cancer cell line SGC-7901 / CDDP induced by cisplatin and its effect on chemoresistance in gastric cancer cells. Its mechanism. Methods Human gastric cancer cell line SGC-7901 and drug-resistant cell SGC-7901 / CDDP were treated with EGb761, cisplatin alone, and EGb761 in combination with cisplatin. The cells were stained with methyl thiazolyl tetrazolium (MTT) The proliferative activity of the two kinds of cells was detected by flow cytometry. The expression of NIBP, NF-κB P65 mRNA and protein were detected by real-time fluorescence quantitative PCR and Western blot. Results Both cisplatin and EGb761 inhibited the proliferation of both gastric cancer cells in a dose-dependent manner. However, SGC-7901 / CDDP cells were less sensitive to cisplatin than SGC-7901 / CDDP. The combination of EGb761 and cisplatin significantly enhanced the sensitivity of cisplatin and promoted the apoptosis of SGC-7901 and SGC-7901 / CDDP cell lines. The relative expression levels of mRNA and protein in NIBP and NF-|ÊB p65 in SGC-7901 / CDDP cells were significantly higher than that in SGC-7901 cells (P <0.05), and EGb761 significantly inhibited cisplatin-induced NIBP and NF- Expression (P <0.05). Conclusion EGb761 has significant chemosensitivity effect and can reverse the drug resistance of gastric cancer cells and enhance the inhibitory effect of cisplatin on the growth of gastric cancer cells and promote apoptosis. The mechanism of reversing anti-tumor cell resistance and chemosensitivity may be through inhibiting the activity of NF-κB pathway and decreasing the expression of NIBP and NF-κB p65.