地塞米松联合人参皂苷Rh2对鼻咽癌化疗效果的影响  

Effects of Dexamethasone(DEX)and Ginsenoside Rh2(GSRh2) on Nasopharyngeal Carcinoma by Chemotherapy

作　　者：吴慧玲[1] 董盛宇[1] 叶耀耀[1] 周慧[2] 

机构地区：[1]吴川市人民医院五官科,广东吴川524500 [2]广东医学院附属医院耳鼻咽喉科,广东湛江524000

出　　处：《湖北民族学院学报（医学版）》2013年第2期33-36,共4页Journal of Hubei Minzu University(Medical Edition)

摘　　要：目的探讨地塞米松和人参皂苷Rh2对鼻咽癌化疗效果的影响。方法将常规培养的人低分化鼻咽癌细胞CNE-2Z分为空白对照组,单纯紫杉醇处理组,地塞米松预处理+紫杉醇组,地塞米松预处理+人参皂苷Rh2+紫杉醇组。MTT法检测各组细胞的OD值并计算被各处理因素作用后的细胞增殖率。RT-PCR检测细胞中与凋亡有关的基因Cyclin D1和Caspase-12的表达。结果地塞米松对紫杉醇处理后的CNE-2Z细胞中凋亡基因Caspase-12的上调和原癌基因cyclinD1的下调均产生显著的抑制,紫杉醇诱导的细胞凋亡现象部分被地塞米松所逆转,导致CNE-2Z细胞的存活率增高。而加入了人参皂苷Rh2后,地塞米松的这种逆转效应被部分抑制。结论地塞米松降低了CNE-2Z细胞对化疗药物紫杉醇的敏感性。而人参皂苷Rh2能够对抗地塞米松的这种效应,部分恢复了肿瘤细胞对紫杉醇的敏感性。Objective To investigate the influence of mechanism of dexamethasone（DEX） and ginsenoside Rh2 （GSRh2）on tumor celIs-CNE-2Z by Paclitaxel chemotheraping.Metheds Na- sopharyngeal carcinoma cell CNE-2Z were treated with Paclitaxel or DEX pretreatment, or combined with GSRh2. The cell proliferation was measured by the Mq-I--assay; Expression of Caspase-12 and cyclin D1 were detected by RT-PCR for mechanism of DEX and GS in cellular Apoptosis signaling pathway.Results DEX reduced the effect of Paclitaxel-induced proliferation inhibition and apoptosis induction in CNE-2Z cells. On the other hand, after combined with GS Rh2, the tumor cells sensitivity to the Paclitaxel was partial restoration. Conclusion DEX could inhibit the effect of the growth inhibition and apoptosis induction by the chemotherapeutic drugs Paclitaxel, but GSRh2 could reverse these effects and restore the sensitivity of CNE-2Z cells to Paclitaxel.

关 键 词：鼻咽癌化疗 紫杉醇 糖皮质激素 人参皂苷 

分 类 号：R739.6[医药卫生—肿瘤]