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作 者:高天勤[1] 李欣[2] 董圣军[1] 程春雷 史荣军 贾龙[1] 王健[1] 刘宝辉[1] GAO Tianqin;LI Xin;DONG Shengjun;CHENG Chunlei;SHI Rongjun;JIA Long;WANG Jian;LIU Baohui(Binzhou Medical University Hospital,Binzhou 256603,China;Binzhou People′s Hospital, Binzhou 255610,China;Shandong Institute of Food and Drug Control,Jinan 250101,China;People′s Hospital of Yangxin County,Yangxin 251800,China)
机构地区:[1]滨州医学院附属医院,山东滨州256603 [2]滨州市人民医院,山东滨州255610 [3]山东省食品药品检验研究院,山东济南250101 [4]阳信县人民医院,山东阳信251800
出 处:《药学研究》2019年第4期198-200,204,共4页Journal of Pharmaceutical Research
摘 要:目的观察芍药苷(paeoniflorin,PF)对人上皮性卵巢癌HO8910细胞增殖、凋亡及迁移能力的影响,并探讨其可能的作用机制。方法培养人上皮性卵巢癌HO8910细胞,随机分为对照组、芍药苷低剂量组、芍药苷中剂量组、芍药苷高剂量组。芍药苷低、中、高剂量组分别在加入0.5、1与2 mg·mL^(-1)芍药苷的DMEM培养液中培养48 h。采用噻唑蓝(MTT)法检测HO8910细胞增殖抑制率;TUNEL染色法检测细胞凋亡率;细胞划痕实验检测HO8910细胞迁移率;免疫蛋白印迹技术(Western blot)分析核因子-κB(NF-κB) p56、Bcl-2、caspase-3蛋白的表达。结果与对照组相比,芍药苷对HO8910细胞增殖、迁移率有明显的抑制作用并促进其凋亡(P<0.05),这种作用呈现剂量依赖性;芍药苷处理组细胞内caspase-3表达水平较对照组明显升高(P<0.05),Bcl-2、核因子-κB p56表达水平较对照组明显降低(P<0.05),且呈现剂量依赖性(P<0.05)。结论芍药苷可明显抑制HO8910细胞的增殖,诱导其凋亡;其机制部分可能与阻断核因子-κB通路有关。ObjectiveTo investigate the effects of paeoniflorin(PF) on proliferation,apoptosis and migration of ovarian cancer cells HO8910.MethodsThe ovarian cancer cells HO8910 were cultured in vitro,and then the cells were divided into control group,low-dose,middle-dose,and high-dose PF groups.The cells in the drug groups were treated with 0.5,1,2 mg·mL^-1 of PF for 48 h,and control group were only cultured in vitro with 0.01% DMSO for 48 h.MTT was used to detected the effects of PF on proliferation of HO8910 cells;The apoptosis rate of HO8910 was detected by TUNEL;The cell scratch test was used to detected the effects of PF on cell migration;The indicator were detected by Western blot,which the expression of nuclear factor-kappaB (NF-κB),caspase-3,B-lymphocyte/leukemia -2 (Bcl-2) protein.ResultsCompared with HO8910 cells of control groupPaeoniflorin restrained cell proliferation,migration ability,and induced apoptosis of HO8910 cells in a dose-dependent manner( P <0.05).The expression of NF-κB p56,Bcl-2 were distinctly down-regulated ( P <0.05),while the expression of caspase-3 was distinctly up-regulated ( P <0.05),and in a dose dependent( P <0.05).ConclusionThe PF can inhibit the proliferation and migration of ovarian cancer cell lines and promote its apoptosis,which might be partly related to inhibit NF-κB activation.
关 键 词:芍药苷 细胞增殖 细胞凋亡 细胞迁移 核因子-ΚB信号通路
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