Study on apoptosis of human lung adenocarcinoma cell line A549/DDP induced by ginsenoside Rh₂ in vitro / 中国肺癌杂志

ABSTRACT

<p><b>BACKGROUND</b>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.</p><p><b>METHODS</b>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.</p><p><b>RESULTS</b>(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).</p><p><b>CONCLUSIONS</b>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.</p>