摘要
背景与目的肺癌已成为人类癌症主要死亡原因之一。从植物中开发抗肿瘤药物是国内外抗肿瘤新药开发的一个热点。本研究的目的是观察人参单体Rh2诱导人肺腺癌A549/DDP细胞系凋亡的作用,并探讨其可能的分子机制。方法体外培养的人肺腺癌A549/DDP细胞经不同浓度梯度的人参单体Rh2干预,分别应用MTT实验观察其对细胞增殖的影响,用流式细胞术检测细胞周期、凋亡指数及相关基因表达的改变,以及用双抗体夹心ELISA法测定细胞上清液sApo-1/Fas浓度变化。结果①人参单体Rh2可抑制A549/DDP细胞的生长,并呈剂量、时间依赖作用。②人参单体Rh2处理A549/DDP细胞24h,实验组凋亡指数显著高于对照组(P<0.001),G0/G1期细胞比例显著高于对照组(P<0.01),S期细胞比例显著低于对照组(P<0.01),G2/M期细胞比例与对照组比较无显著性差异(P>0.05)。③实验组p53、Fas阳性表达率显著高于对照组(P<0.01,P<0.001),Bcl-2阳性表达率显著低于对照组(P<0.001)。④实验组A549/DDP细胞培养上清液于不同时间sApo-1/Fas含量均显著低于对照组(P<0.05)。结论人参单体Rh2具有诱导人肺腺癌A549/DDP细胞凋亡的作用,其分子机制可能是上调p53和Fas及下调Bcl-2的表达、通过Fas/FasL系统途径诱导细胞凋亡。
Background and objective Lung cancer is one of the leading causes of cancer-related death in mankind. To exploit antitumor drug from plant has been a highlight at home and abroad. The aim of this study is to investigate the apoptosis of human lung adenocarcinoma cell line A549/DDP induced by ginsenoside Rh2 （G-Rh2） and to explore its possible molecular mechanism. Methods The growth inhibition effect of G-Rh2 on A549/DDP cells was evaluated by MTT assay. Cell cycle analysis, apoptosis index and tumor related gene expression were detected by flow cytometry. The changes of sApo-1/Fas level in the cell culture supernatant were determined by ELISA method. Results ① G-Rh2 significantly inhibited the growth of A549/DDP cells in a dose-time-de-pendent manner.② After 24 hours＇ treatment with G-Rh2 , apoptosis index of trial group was significantly higher than that of control group （P〈0. 001）. The proportion of cells in G0/G1 phase in trial group was much higher than that in control group （P〈0. 01）, while proportion in S phase in trial group was markedly lower than that in control group （P〈0.01）. There was no significant difference in proportion in G2/M phase between trial group and control group （P〉0.05）. ③ The positive expression rate of p53 and Fas in trial group was significantly higher than that in control group （P〈0.01, P〈0. 001）, while the positive expression rate of Bcl-2 in trial group was significantly lower than that in control group （P〈0. 001）. ④ The level of sApo-1/Fas in A549/DDP cell culture supernatant in trial group was remarkably lower than that in control group （P〈0. 05）. Conclusion G-Rh2 can induce the apoptosis of A549/DDP cells. Its molecular mechanism may be up-regulating expression of p53 and Fas and down-regulating expression of Bcl-2.
出处
《中国肺癌杂志》
CAS
2005年第4期257-260,共4页
Chinese Journal of Lung Cancer
