›› 2011, Vol. 23 ›› Issue (1): 50-053.doi: 10.3969/j.issn.1004-616x.2011.01.013

• 肿瘤防治 • 上一篇    下一篇

明日叶查尔酮对小鼠肝癌细胞Caspase-3和Bax蛋白表达的影响

孟 扬,钟进义*,孙 赫   

  1. 青岛大学医学院,山东 青岛
  • 收稿日期:2010-09-10 修回日期:2010-11-18 出版日期:2011-01-30 发布日期:2011-01-30
  • 通讯作者: 钟进义

Effects of Ashitaba chalcone on Caspase-3 and Bax protein expressions of mouse hepatocarcinoma cells

MENG Yang,ZHONG Jin-yi*,SUN He   

  1. Medical College of Qingdao University, Qingdao Shandong, China
  • Received:2010-09-10 Revised:2010-11-18 Online:2011-01-30 Published:2011-01-30
  • Contact: ZHONG Jin-yi

摘要: 研究明日叶查尔酮(Ashitabe chalcone, AC)对小鼠H22肝癌细胞Caspase-3和Bax蛋白表达的影响。 方法: 将50只荷H22肝癌小鼠随机分为AC不同剂量实验组(5、20、40 mg/kg),阴性对照组和环磷酰胺(cytoxan, CTX)阳性对照组,共5组,每组10只。AC实验组小鼠每天分别按不同的剂量灌胃,阴性对照组小鼠给予生理盐水灌胃,CTX组隔天腹腔注射CTX 20 mg/kg,10 d后处死小鼠,取瘤组织测定瘤质量、抑瘤率,并采用免疫组化法检测各组小鼠肿瘤细胞Caspase-3和Bax蛋白的表达,用MTT法检测各组小鼠肿瘤细胞增殖活性。 结果:阴性对照组小鼠肿瘤细胞Caspase-3和Bax阳性细胞表达率分别为5.00% 和4.68%,AC 40 mg/kg剂量组分别为38.52% 和35.76%,均高于阴性对照组(P < 0.05);阴性对照组肝癌细胞增殖活性为1.135±0.032,AC 40 mg/kg剂量组为0.716±0.018,低于阴性对照组(P< 0.05)。AC 20、40 mg/kg剂量组平均瘤质量均明显低于阴性对照组(P< 0.05)。 结论: 明日叶查尔酮可上调Caspase-3和Bax蛋白的表达且具有抑制肿瘤细胞增殖作用。

关键词: 明日叶查尔酮, 肝癌, Caspase-3, Bax

Abstract: To investigate the effects of Ashitaba chalcone (AC) on Caspase-3 and Bax protein expressions in mouse hepatocarcinoma cells. METHODS: Fifty mice inoculated with hepatocarcinoma 22 cells were divided into five groups, 10 mice per group. 5,20,40 mg/kg AC were given daily by mouth to form low, medium and high dose groups, respectively. Normal saline by mouth was given to the tumor control group. 20 mg/kg cytoxan(CTX) by injection every other day were given to the CTX group.10 days later, all mice were sacrificed. The levels of the Caspase-3 and Bax protein expressions were measured by immunohistochemistry, and the proliferation activity of hepatocarcinoma cells was determined by MTT assay. RESULTS: The expressions level of Caspase-3 and Bax protein in tumor control group were 5.00% and 4.68%, respectively, and those of the high-dose group were 38.52% and 35.76%. The differences between two groups were significant (P<0.05). The cell proliferation activity of tumor control group and high-dose group were 1.135±0.032 and 0.716±0.018, respectively. The difference was significant (P<0.05). The rumor weight in AC 20, 40 mg/kg were significantly lower than that in tumor control group (P<0.05). CONCLUSION: AC could induce the expressions of Caspase-3 and Bax protein.

Key words: Ashitaba chalcone, hepatocarcinoma, Caspase-3, Bax