中国癌症杂志 ›› 2015, Vol. 25 ›› Issue (1): 31-37.doi: 10.3969/j.issn.1007-3969.2015.01.006

• 论著 • 上一篇    下一篇

冬凌草甲素对胰腺癌细胞骨架蛋白F-actin的影响

刘军楼,沈洪,徐力,杨继兵,于希忠,孙志岭   

  1. 南京中医药大学第一临床医学院,江苏 南京,210046
  • 出版日期:2015-01-30 发布日期:2015-05-08
  • 通信作者: 沈洪 E-mail:shenhong999@163.com
  • 基金资助:
    江苏省中医药局课题资助项目(LZ11196);江苏省高校自然科学基金资助项目(13KJB360011)。

Effects of oridonin on cytoskeletal protein F-actin in human pancreatic carcinoma cells

LIU Junlou, SHEN Hong, XU Li, YANG Jibing, YU Xizhong, SU Zhiling   

  1. Effects of oridonin on cytoskeletal protein F-actin in human pancreatic carcinoma cells
  • Published:2015-01-30 Online:2015-05-08
  • Contact: SHEN Hong E-mail: shenhong999@163.com

摘要:
背景与目的:中医药治疗肿瘤不良反应低且疗效显著,在防治胰腺癌方面有较大的潜力与优势,日益受到国内、外医学界的关注。本研究观察中草药冬凌草的有效成分冬凌草甲素对人胰腺癌SW1990凋亡及细胞骨架蛋白F-actin的影响。方法:以不同浓度的冬凌草甲素作用于体外培养的SW1990细胞,采用MTT法检测细胞生长抑制率,DAPI染色法染色后荧光显微镜观察细胞核凋亡、流式细胞仪检测细胞凋亡率,激光共聚焦显微镜观察F-actin形态学变化。结果:冬凌草甲素对人胰腺癌SW1990细胞具有明显的增殖抑制作用,荧光显微镜见到典型的凋亡形态学改变。流式细胞仪检测结果显示,25、50 μmol/L冬凌草甲素给药组早期凋亡的百分率显著高于对照组(3.78±0.46,9.51±0.63 vs 0.73±0.06,P<0.05),晚期凋亡和坏死细胞的百分率也显著高于未给药组(14.40±1.78,20.53±2.54 vs 4.16±0.31,P<0.05)。细胞骨架蛋白F-actin呈现解聚状态。结论:冬凌草甲素可抑制胰腺癌SW1990细胞增殖,促进肿瘤细胞凋亡,其作用机制可能是药物引起了细胞骨架蛋白F-actin解聚。

关键词:  冬凌草甲素, 胰腺癌, 增殖抑制, 凋亡, 细胞骨架蛋白

Abstract:
Background and purpose: Traditional Chinese medicine with notable effect and little adverse reaction is increasingly concerned about the medical profession because of its great potential and advantage in treating pancreatic carcinoma. In this experiment, we studied the effects of oridonin on apoptosis and cytoskeletal protein F-actin in human pancreatic carcinoma SW1990 cells. Methods: SW1990 cells in culture medium were treated with different concentrations of oridonin. The inhibitory rate of the cells was measured by MTT assay. Morphology of cell apoptosis was observed by DAPI stain and cell apoptotic rate was detected by flow cytometry (FCM). The morphological changes of F-actin were observed by laser confocal microscopy. Results: The growth of human pancreatic carcinoma SW1990 cells was significantly inhibited by oridonin. Apoptosis morphological changes including condensation of chromatin and nuclear fragmentation were observed clearly by DAPI stain. The early apoptotic rate of SW1990 cells treated with 25, 50 μmol/L oridonin was significantly higher than that of the control group (3.78±0.46, 9.51±0.63 vs 0.73±0.06, P<0.05), and the late apoptotic rate and cell necrosis rate were also significantly higher than that of the control group (14.40±1.78, 20.53±2.54 vs 4.16±0.31, P<0.05). F-actin was showed from polymerization to depolymerization after oridonin treatment. Conclusion: Oridonin can obviously inhibit the proliferation and induce apoptosis of SW1990 cells. The mechanisms may involve the depolymerization of F-actin after treatment with oridonin.

Key words: Oridonin, Pancreatic carcinoma, Antiproliferation, Apoptosis, Cytoskeletal protein