摘要
[目的]探讨槐耳清膏对p53基因表达缺失的人肺癌细胞系H1299(p53-null)体外生长化疗敏感性的影响。[方法]应用MTT法、流式细胞仪及克隆形成试验,检测槐耳清膏对H1299生长的影响及对化疗药物(DDP和ADM)敏感性的变化。[结果]槐耳清膏能使H1299细胞体外生长速度明显减慢,其抑制生长的作用具有剂量依赖性。MTT实验提示槐耳清膏使顺铂和阿霉素的IC50值分别减少了4倍和45倍,槐耳清膏(1.0g/L)联合原本没有明显抑制和杀伤作用的化疗药物(1.25μmol/L的顺铂或0.25μmol/L的阿霉素)使H1299细胞生长明显受到抑制。流式细胞术显示槐耳清膏使顺铂诱导的细胞凋亡率从12.8%升高到33.5%(P<0.01),阿霉素诱导的细胞凋亡率从22.7%升高到51.0%(P<0.01)。克隆形成实验显示槐耳清膏能明显降低化疗后细胞的克隆形成数(P<0.01),对顺铂和阿霉素的化疗增效倍数分别为1.9和1.6倍。[结论]槐耳清膏可以抑制人肺腺癌细胞H1299体外生长并提高其对阿霉素、顺铂等化疗药的敏感性,且这种作用不依赖于p53基因。
[Purpose ] To investigate the effect of PS-T on growth in vitro and chemosensitivity of H1299 cells (p53-null) of human lung adenocarcinoma. [Methods] The effect on growth of H1299 cells with PS-T was observed by MTT assay. The change of chemosensitivity on cisplatin(DDP), adriamycin(ADM) was observed by flow cytometry and colony formation assay. [Results] PS-T significantly inhibited growth of H1299 cells in vitro and the antiproliferatitive effect occurred in a dose dependent manner. MTT assay showed that the ICso values for DDP and ADM were reduced to approximate 4 and 45 fold respectively when PS-T combined with chemotherapeutic agent. Chemotherapeutic drugs (1.25μmol/L DDP or 0.25μmol/L ADM)without inhibition essentially suppressed growth of H1299 cells markedly when they combined with PS-T (1.0g/L). The DDP-induced apoptosis rate increased from 12.8% to 33.5%(P〈0.01)and the ADM-induced apoptosis rate increased from 22.7% to 51.0% (P〈0.01)when they combined with PS-T by flow cytometry. In colony-formation assays, the colony number acted by chemotherapeutic agents significantly decreased when they combined with PS-T(P〈0.01 ). The sensitive enhancement ratios were 1.9 and 1.6 for DDP and ADM, respectively. [Conclusion] PS-T is capable of inhibiting the growth in vitro of human lung adenocarcinoma cells H1299 and enhancing its sensitivity to chemotherapeutic agents(DDP or ADM). This role is not depend on p53 gene.
出处
《中国肿瘤》
CAS
2008年第12期1053-1056,共4页
China Cancer
关键词
槐耳清膏
肺肿瘤
化疗敏感性
P53基因
polysaccharide of trametes robiniophila murr (PS-T), lung neoplasms
chemotherapeutic sensitivity
p53 gene