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9顺维A酸对人肺腺癌细胞A2增殖及凋亡影响的实验研究

Effects of 9-Cis-Retinoic Acid on the Proliferation and Apoptosis of Human Lung Cancer Cell Line A2
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摘要 研究9顺维A酸(9-cis RA)抑制肺腺癌细胞A2增殖及诱导凋亡的作用并初步探讨其作用机制。体外培养A2细胞,随机分为4组,实验组加9-cis RA使其终浓度为1、5、10μmol/L,对照组加入二甲亚砜使其终质量分数为0.1%,采用MTT法检测各组A2细胞增殖情况;使用流式细胞术(flow cytometry,FCM)分析药物作用后各组细胞的凋亡率;用逆转录-聚合酶链反应(RTPCR)检测各组细胞bax、fas、bcl-2基因的变化。9顺维A酸对人肺癌细胞株A2增殖均有明显的抑制作用(P<0.01),实验组中细胞凋亡发生率显著增高(P<0.05),且随着浓度的升高抑制作用和凋亡率也随之提高。实验组bax m RNA、fas m RNA表达显著高于对照组,差异有统计学意义(P<0.01);实验组bcl-2 m RNA表达显著低于对照组,差异具有统计学意义(P<0.01)。结论 9-cis RA具有明显的抗肺腺癌细胞A2增殖的作用,其机制可能通过上调bax、fas基因和下调bcl-2基因表达、诱导细胞凋亡有关。 The study aimed to explore the mechanism of 9-cis-retinoic acid(9-cis RA) inhibiting proliferation and inducing apoptosis in human lung cancer cell line A2.Cultured A2 cells were randomly divided into four groups,the experimental group received 9-cis RA to a final concentration of 1,5 or 10 μmol/L,and the control group was added dimethyl sulfoxide to a final concentration of0.1%. The MTT method was used for the determination of cell proliferation,flow cytometry(FCM)for the analysis of apoptosis,and reverse transcription-polymerase chain reaction(RT-PCR) for the expression changes of bax,fas and bcl-2 genes. Results showed that 9-cis RA significantly inhibited the cell proliferation(P<0.01) and the incidences of apoptosis in the experimental groups were significantly higher(P<0.05),which depended on the concentration of 9-cis RA.The m RNA expressions of bax and fas genes in the experimental groups were significantly higher(P<0.01)whereas the bcl-2m RNA expressionwas significantly lower than the control group(P<0.01).Therefore,9-cis RA significantly inhibitsthe proliferation of human lung cancer cell line A2,which may be related to the increased expressions of bax and fas genes and the decreased expression of bcl-2 gene,and then induced apoptosis.
出处 《食品与生物技术学报》 CAS CSCD 北大核心 2015年第7期779-783,共5页 Journal of Food Science and Biotechnology
基金 无锡市医院管理中心重大项目(YGZX1210)
关键词 9-顺维A酸 肺癌 细胞增殖 细胞凋亡 9-cis-retinoic acid,lung cancer,cell proliferation,apoptosis
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