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机构地区:[1]重庆市肿瘤研究所妇产科,重庆400030 [2]重庆市肿瘤研究所临床检验中心,重庆400030
出 处:《中国药房》2013年第19期1756-1759,共4页China Pharmacy
摘 要:目的:研究紫杉醇(PTX)联合固体脂质纳米姜黄素(SLN-Cur)对人卵巢癌HO-8910细胞体外生长的抑制作用。方法:试验分为4组,即阴性对照(仅含正常生产的HO-8910细胞)、PTX(2.5μmol/L)、SLN-Cur(10μmol/L)、PTX+SLN-Cur(2.5μmol/L+10μmol/L)组。MTT法测定HO-8910细胞增殖抑制率,透射电镜观察HO-8910细胞凋亡超微结构变化,流式细胞仪检测细胞凋亡率与细胞周期分布变化,免疫组化法检测凋亡相关基因蛋白酶的表达。结果:PTX、SLN-Cur、PTX+SLN-Cur均可显著抑制人卵巢癌HO-8910细胞的增殖,其中PTX+SLN-Cur作用最强。与阴性对照组比较,PTX、SLN-Cur、PTX+SLN-Cur组凋亡率显著增加,S期细胞比例逐渐降低,G2/M期细胞比例逐渐增高,MMP-9表达减弱,TIMP-2表达增强,其中PTX+SLN-Cur组表现更显著。结论:SLN-Cur对人卵巢癌HO-8910细胞具有较好的体外抑制效果,与PTX联合化疗有增效减毒作用,其机制可能与下调MMP-9表达及上调TIMP-2表达而诱导细胞凋亡有关。OBJECTIVE : To study of paclitaxel (PTX) combined with solid lipid nanoparticles of curcumin (SLN-Cur) on the growth inhibition of human ovarian cancer HO-8910 cells in vitro. METHODS:The experiment was divided into 4 groups, the negative control (containing only the normal production of riO-8910 cells), PTX (2.5 μmol/L), SLN-Cur (10/zmol/L), PTX+ SLN-Cur (2.5 lamol/L+ 10 μmol/L) group. Determination of inhibitory rate of HO-8910 cell proliferation by MTT method, the ultrastructural changes of apoptosis of HO-8910 cells were observed by transmission electron microscope, and detected the apoptosis rate and cell cycle distribution of flow cytometry, immunohistochemistry method was used to detect the expression of apoptosis related gene protein. RESULTS: PTX, SLN-Cur, PTX+ SLN-Cur can significantly inhibit the proliferation of human ovarian cancer HO-8910 cells, in which PTX+ SLN-Cur had the strongest effect. Compared with the negative control group, PTX, SLN-Cur, PTX+ SLN-Cur group significantly increased, apoptosis rate, the percentage of S phase ceils decreased, the percentage of GJM phase cells gradually increased, MMP-9 expression decreased, increased the expression of TIMP-2. The PTX+ SLN-Cur group showed more significant. CONCLUSIONS: SLN-Cur had better inhibition effect in vitro on human ovarian cancer HO-8910 cells, attenuated synergistic effect in combination with PTX chemotherapy, and to investigate the possible mechanism of MMP-9 expression and up-regulation of TIMP-2 expression and induction of apoptosis.
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