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作 者:史晓娜 徐霞 谢闺娥 SHI Xiaona;XU Xia;XIE Guie(KingMed School of Laboratory Medicine,Guangzhou Medical University,Guangdong Province,Guangzhou 510182,China)
机构地区:[1]广州医科大学金域检验学院,广东广州510182
出 处:《中国医药导报》2021年第1期18-21,F0004,共5页China Medical Herald
基 金:广东省自然科学基金项目(2017A030313906);广州医科大学大学生实验室开放项目(2018-22)。
摘 要:目的研究雷公藤红素对MDA-MB-231乳腺癌细胞的抗肿瘤作用及其机制。方法用MTT比色法检测雷公藤红素对MDA-MB-231生长的影响,并计算其半数抑制浓度(IC50)。其机制研究的实验均分为两组:对照组和处理组。对照组细胞未经任何处理,处理组细胞用2.0μmol/L雷公藤红素作用后,Annexin V-FITC荧光染色及TUNEL染色法检测凋亡细胞比率;免疫印迹法分析p-Akt、Akt、Survivin和Bcl-xL的蛋白表达水平。结果雷公藤红素能抑制MDA-MB-231的生长,作用48 h的IC50为0.93μmol/L。处理组Annexin V-FITC染色阳性的凋亡细胞比率和TUNEL染色阳性细胞比率均高于对照组,差异均有统计学意义(均P <0.05)。与对照组比较,处理组p-Akt、Survivin和Bcl-xL的蛋白表达下降,差异均有统计学意义(均P <0.05);两组Akt总蛋白表达比较,差异无统计学意义(P> 0.05)。结论雷公藤红素通过调节Akt信号通路诱导MDA-MB-231凋亡的发生,进而抑制MDA-MB-231细胞的生长。Objective To study the antitumor effect of tripterine on MDA-MB-231 breast cancer cells and its mechanism. Methods The effect of tripterine on the growth of MDA-MB-231 was determined by MTT colorimetric method,and its half maximal inhibitory concentration(IC50) was calculated. The experiments on its mechanism were divided into two groups: control group and treatment group. The control group cells were untreated. After the treatment group cells were treated with 2.0 μmol/L tripterine, the ratio of apoptotic cells was determined by Annexin V-FITC fluorescence staining and TUNEL staining. The protein expression levels of p-Akt, Akt, Survivin and Bcl-xL were analyzed by Western blot. Results Tripterine inhibited the growth of MDA-MB-231 with IC50 of 0.93 μmol/L for 48 h. The ratio of Annexin V-FITC staining positive apoptotic cells and the ratio of TUNEL staining positive cells in the treatment group were higher than those in the control group, with statistically significant differences(all P < 0.05). Compared with the control group, p-Akt, Survivin and Bcl-xL protein expressions in the treatment group decreased, and the differences were statistically significant(all P < 0.05). Comparison of Akt total protein expression between the two groups showed no statistically significant difference(P > 0.05). Conclusion Tripterine induces the apoptosis of MDA-MB-231 cells by regulating the Akt signaling pathway, and then inhibits the growth of MDA-MB-231 cells.
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