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姜黄素对胰腺癌细胞株生长的抑制作用及可能机制
引用本文:宫爱霞 关凤林 刘敏 于春红 吕申. 姜黄素对胰腺癌细胞株生长的抑制作用及可能机制[J]. 胰腺病学, 2004, 4(4): 218-222
作者姓名:宫爱霞 关凤林 刘敏 于春红 吕申
作者单位:[1]大连医科大学附属一院消化科,辽宁116011 [2]大连医科大学附属二院中心实验室,辽宁116011
摘    要:目的研究姜黄素对胰腺癌细胞增殖的体外抑制作用.探讨其抗癌作用的分子生物学机制。方法MTT法、Annexln V-FITC/PI双染法、细胞周期分析法、透射电镜等方法检测姜黄素对Pan02细胞生长和凋亡的影响.RT—PCR检测姜黄素对Pan02细胞Bax,Bcl-2,COX2,Bak.Survfvin mRNA的表达。结果(1)姜黄素抑制Pan02细胞生长呈量效关系;(2)姜黄素处理组细胞周期发生改变.G2/M期细胞比例增多、S期细胞比例减少;(3)姜黄素处理组细胞发生凋亡.表现为凋亡细胞比例增多,形态上出现明显细胞凋亡:(4)姜黄素处理组Pan02细胞Bcl-2和Bak mRNA表达水平显著下降.COX-2.Bax mRNA表达水平显著升高,Survivin mRNA的表达水平没有变化。结论姜黄素能够抑制Pan02细胞增殖,它可改变细胞周期、诱导细胞凋亡.Bcl-2家族而不是IAP家族(至少不是Survivin)参与了Pan02细胞的凋亡过程。

关 键 词:姜黄素 胰腺癌 癌细胞 细胞生长 抑制作用 抗癌作用 细胞死亡
修稿时间:2004-06-29

Inhibitory effect of Curcumin on pancreatic carcinoma cell line and possible mechanisms
GONG Ai- Xia,GU AN Feng-Lin,LIU Min,YU Chun-Hong,LV Shen. Inhibitory effect of Curcumin on pancreatic carcinoma cell line and possible mechanisms[J]. Chinese JOurnal of Pancreatology, 2004, 4(4): 218-222
Authors:GONG Ai- Xia  GU AN Feng-Lin  LIU Min  YU Chun-Hong  LV Shen
Affiliation:GONG Ai- Xia,GU AN Feng-Lin,LIU Min,YU Chun-Hong,LV Shen. Department oj Gastroenterology First Affiliated Hospital,Dalian Medical University,Dalian 116011,LN,China
Abstract:Objective To study the inhibitory effect of Curcumin on cell proliferation of pancreatic carcinoma in vitro, and discuss the molecular biologic mechanism of its anti-carcinoma function. Methods Influence of Curcumin on proliferation and apoptosis of Pan02 cells was evaluated by MTT, Annexin V-FITC/PI double staining, cell cycle-phase analysis and transmission electron microscopy; the expression of Bax, Bcl-2, COX-2. Bak and Survivin mRNA in Pan02 cell treated with Curcumin was assessed by RT-PCR. Results (1)The inhibitory effect of Curcumin on Pan02 cell proliferation was found to be in a dose-dependent manner; (2)Cell cycle change was observed in the group treated with Curcumin; the percentage of cells in G2/M stage increased, and that in S stage decreased; (3)Cell apoptosis was observed in the group treated with Curcumin, which was represented by the increased percentage of apoptotic cells and presence of cells with marked morphological change; (4) The expression of Bcl-2 and Bak mRNA in Pan02 cells treated with Curcumin down-regulated significantly, while the level of COX-2 and Bax mRNA up-regulated significantly. There was no change in Survivin mRNA expression. Conclusions Curcumin inhibited the proliferation of Pan02 cells by changing cell cycle and inducing apoptosis. It is the BCL-2 family, not the IAP family (at least not Survivin) ,that participates in the apoptosis of Pan02 cells.
Keywords:Curcumin  Pancreatic neoplasms  Tumor cells   cultured  Drug action  Cell death
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