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蔓荆子黄素对人非小细胞肺癌细胞H322的作用及机制研究
引用本文:李遂新1,雷光焰2,马晓军1,杨得振3,徐宗君1,陈正浤1. 蔓荆子黄素对人非小细胞肺癌细胞H322的作用及机制研究[J]. 现代肿瘤医学, 2020, 0(7): 1072-1076. DOI: 10.3969/j.issn.1672-4992.2020.07.004
作者姓名:李遂新1  雷光焰2  马晓军1  杨得振3  徐宗君1  陈正浤1
作者单位:1.陕西中医药大学,陕西 咸阳 712046;2.陕西省肿瘤医院,陕西 西安 710061;3.陕西中医药大学附属医院,陕西 咸阳 712000
基金项目:陕西省自然科学基础研究计划项目(编号:2016JM8117)
摘    要:目的:探究蔓荆子黄素对人非小细胞肺癌细胞H322增殖和周期的影响及机制。方法:选择体外培养的人非小细胞肺癌H322细胞,给不同浓度(0,1,10,20,40 μmol/L)蔓荆子黄素溶液作用不同时间(24 h,48 h,72 h)后,采取MTT法检测细胞的增殖情况、流式细胞仪检测细胞周期、Western blot法检测CDK1、c-myc和survivin 基因的表达情况。结果:不同浓度组的蔓荆子黄素溶液作用H322细胞(24 h,48 h,72 h)后均能抑制其增殖(P<0.05),且表现出剂量、时间依赖性;蔓荆子黄素通过影响H322细胞的增殖,使得细胞周期阻滞在G2/M期,同时发现c-myc和survivin 的表达与蔓荆子黄素浓度成负相关,CDK1的表达随着蔓荆子黄素浓度的升高先升高后降低。结论:蔓荆子黄素可能通过抑制CDK1、c-myc和survivin 的表达,阻滞细胞周期在G2/M期,进而抑制人非小细胞肺癌细胞H322的增殖并促进凋亡。

关 键 词:蔓荆子黄素  非小细胞肺癌  增殖  凋亡  CDK1  c-myc  survivin

The effects and mechanism of vitexicarpin on human non-small cell lung cancer cell H322
Li Suixin1,Lei Guangyan2,Ma Xiaojun1,Yang Dezhen3,Xu Zongjun1,Chen Zhenghong1. The effects and mechanism of vitexicarpin on human non-small cell lung cancer cell H322[J]. Journal of Modern Oncology, 2020, 0(7): 1072-1076. DOI: 10.3969/j.issn.1672-4992.2020.07.004
Authors:Li Suixin1  Lei Guangyan2  Ma Xiaojun1  Yang Dezhen3  Xu Zongjun1  Chen Zhenghong1
Affiliation:1.Shaanxi University of Chinese Medicine,Shaanxi Xianyang 712046,China;2.Shaanxi Cancer Hospital,Shaanxi Xi'an 710061,China;3.Affiliated Hospital of Shaanxi University of Chinese Medicine,Shaanxi Xianyang 712000,China.
Abstract:Objective:To investigate how vitexicarpin will influence the multiplication and cycle of the human non-small cell lung cancer (NSCLC) cell H322.Methods:Select human non-small cell lung cancer cell H322 cultured in vitro,influence it with the vitexicarpin solutions at different densities of 0,1,10,20,40 μmol/L for different time periods (24 h,48 h,72 h),and then examine the multiplication of the cell with the MTT method.The cell cycle was detected by the flow cytometer and the expression of CDK1,c-myc and survivin genes were detected by the Western blot method.Results:The vitexicarpin solutions in different density groups can all suppress the multiplication of the cell H322 (24 h,48 h,72 h) after acting on it (P<0.05),with the dependence on dosage and time.The vitexicarpin will intercept the cell cycle at the G2/M phase by influencing the multiplication of the cell H322,and the expression of c-myc and survivin showed a negative correlation with the densities of the vitexicarpin,the expression of CDK1 first increased and then decreased with the increase of vitexicarpin.Conclusion:The vitexicarpin can stop the cell cycle at the G2/M phase by suppressing the expressions of CDK1,c-myc and survivin,thereby further curbing the multiplication of the human non-small cell lung cancer H322 and promoting its apoptosis.
Keywords:vitexicarpin   non-small cell lung cancer   proliferation   apoptosis   CDK1   c-myc   survivin
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