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作 者:赵玲俊[1] 高松[2] 徐子琴 姜丽真 王大庆[1] ZHAO Lingjun;GAO Song;XU Ziqin;JIANG Lizhen;WANG Daqing(Internal Medicine - Oneology, Harrison International Peace Hospital, Hengshui 053000, Hebei, China;Pharmaey Department, Harrison International Peace Hospital, Hengshui 053000, Hebei, China)
机构地区:[1]哈励逊国际和平医院肿瘤内科,河北衡水053000 [2]哈励逊国际和平医院药剂科,河北衡水053000
出 处:《辽宁中医杂志》2018年第4期780-783,共4页Liaoning Journal of Traditional Chinese Medicine
摘 要:目的:本研究旨在研究和探讨康艾注射液对于人类乳腺癌细胞增殖的抑制作用及其分子机制研究,从而为临床上应用康艾注射液治疗乳腺癌提供一定的理论依据。方法:本研究利用体外细胞实验,研究了康艾注射液对于乳腺癌细胞的增殖、克隆形成以及凋亡的影响。并且采用Western blot的方法检测了乳腺癌细胞中p-AKT蛋白和p-AMPK蛋白的表达。结果:人类乳腺癌细胞MDA-MB-435S、MDA-MB-231、SK-BR-3以及HCC-1937经康艾注射液干预48h后,细胞活性较对照组分别减少(19.49±2.92)%,(45.41±7.95)%,(53.84±5.53)%,(64.04±4.36)%。经康艾注射液处理2周后,人类乳腺癌细胞MDA-MB-435S、MDA-MB-231、SK-BR-3以及HCC-1937的细胞克隆数较正常对照组均明显减少。康艾注射液在人类乳腺癌细胞诱导细胞凋亡。其对于MDA-MB-435S、MDA-MB-231、SK-BR-3以及HCC-1937的凋亡诱导率为(11.67±1.17)%,(17.54±1.83)%,(15.45±1.55)%,(15.54±1.57)%。Western blot显示,康艾注射液处理细胞后磷酸化的AKT蛋白(p-AKT)表达降低,而AMPK(p-AMPK)蛋白表达增加。结论:康艾注射液可以抑制乳腺癌细胞的增殖,促进细胞凋亡。这可能是通过AMPK/m TOR信号传导通路而达成的。Objective: To study and explore the inhibitory effect of Kang’ai Injection on the proliferation of human breast cancer cells and its molecular mechanismso as to provide a theoretical basis for the clinical application of Kang’ai Injection in the treatment of breast cancer. Methods: In this study,the effects of Kang’ai Injection on the proliferation,clonal formation and apoptosis of breast cancer cells were studied by using in vitro cell experiments. Western blot was used to detect the expressions of p-AKT protein and p-AMPK protein in breast cancer cells. Results: The activities of MDA-MB-435 S,MDA-MB-231,SK-BR-3 and HCC-1937 were decreased by( 19. 49 ± 2. 92) %,( 45. 41 ± 7. 95) %,( 53. 84 ± 5. 53) % and( 64. 04 ± 4. 36) %,respectively after 48 days of Kang’ai Injectionintervention. The cell clones of human breast cancer cells MDA-MB-435 S,MDA-MB-231,SK-BR-3 and HCC-1937 were significantly decreased after 2 weeks of treatment with Kang’ai Injection. Kang’ai Injection in human breast cancer cells induced apoptosis. The apoptosis rate of MDA-MB-435 S,MDA-MB-231,SK-BR-3 and HCC-1937 was( 11. 67 ± 1. 17) %,( 17. 54 ± 1. 83) %,( 15. 45 ± 1. 55) % and( 15. 54 ± 1. 57) % respectively. Western blot showed that the expression of phosphorylated AKT protein( p-AKT) was decreased and the expression of AMPK( p-AMPK) protein was increased after treatment with Kang’ai Injection. Conclusion: Kang’ai Injection can inhibit the proliferation of breast cancer cells and promote cell apoptosis. This may be achieved through the AMPK/m TOR signaling pathway.
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