天津医药

• 论著 •    下一篇

蝎毒多肽提取物对人膀胱癌T24细胞增殖抑制作用的研究*

侯毅1,龙俊任1,张平2,3,龙兵1,陈晓波1,董自强2   

  1. 1. 三峡大学第一临床医学院
    2. 三峡大学第一临床医学院泌尿外科
    3. 1First Clinical Medical College CTGU, Yichang Central Hospital，Hubei 443000, China
  • 收稿日期:2012-05-03 修回日期:2012-10-17 出版日期:2013-03-15 发布日期:2013-03-15
  • 通讯作者: 侯毅

  • Received:2012-05-03 Revised:2012-10-17 Published:2013-03-15 Online:2013-03-15
  • Contact: HOU Yi

PDF (PC)

934

摘要：

【摘要】目的 探讨蝎毒多肽提取物(PESV) 对人膀胱癌T24细胞增殖的抑制作用及其机制。方法 采用体外培养法培养T24细胞，应用MTT法检测对照组和实验组（不同浓度PESV）处理膀胱癌T24细胞后的增殖变化；倒置显微镜观察其对T24细胞形态的影响；RT-PCR检测实验组（低剂量、中剂量及高剂量）BAX和Bcl-2的mRNA的表达变化。结果：PESV能显著抑制T24细胞的增殖，呈现时间和剂量依赖性，差异具有统计学意义（P < 0.01），24 h抑制率接近50% 的T24细胞生长浓度为75 mg/L；低、中及高浓度PESV均可致T24细胞生长明显抑制，出现典型细胞凋亡形态；和对照组比较，实验组BAX mRNA和BAX/Bcl-2 mRNA表达升高，Bcl-2 mRNA表达下降，差异有统计学意义（P < 0.01）。结论 PESV对膀胱癌T24细胞具有明显抑制作用，其诱导T24细胞凋亡的作用可能与上调BAX和下调Bcl-2 的表达有关。

关键词: 蝎毒多肽提取物, 膀胱癌, T24细胞

Abstract: [Abstract] Objective To investigate the effect of polypeptide extract from scorpion venom (PESV) on the proliferation of human bladder carcinoma T24 cells, and the mechanism thereof. Methods  T24 cells were cultured in vitro and treated with different concentration of PEST. The proliferation of cells was detected by MTT assay. The variation of cell morphology was observed by the invented microscope. RT-PCR was used to detect the variation of BAX mRNA and Bcl-2 mRNA in low dose, middle dose and high dose PEST groups.Results  PESV significantly inhibited the proliferation of human bladder carcinoma T24 cells in a dose-dependent and time-dependent manner (P < 0.01). The concentration of inhibited half T24 cells was 75 mg/L. The cell apoptosis was observed in different concentrations of PESV groups. Compared with control group, the expressions of BAX and BAX/Bcl-2 mRNA were gradually increased and the expression of Bcl-2 mRNA was gradually decreased with the concentration of PESV increasing (P < 0.01). Conclusion  PESV can inhibit proliferation of human blad? der carcinoma T24 cells and the possible mechanism may be related with the up-regulation of BAX expression and down-reg? ulation of Bcl-2.