| 桦木酮酸抑制PI3K/AKT通路体内抗肿瘤作用研究 |
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| 引用本文： | 张秀娟,韩磊,凌莉莉,李秋实,季宇彬,方桂珍.桦木酮酸抑制PI3K/AKT通路体内抗肿瘤作用研究[J].哈尔滨商业大学学报(自然科学版),2008,24(3):261-264. |
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| 作者姓名： | 张秀娟 韩磊 凌莉莉 李秋实 季宇彬 方桂珍 |
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| 作者单位： | 1. 哈尔滨商业大学,生命科学与环境科学研究发展中心药物研究所,博士后科研工作站,哈尔滨,150076;国家教育部抗肿瘤天然药物工程研究中心,哈尔滨,150076
2. 东北林业大学,材料工程与技术学院,哈尔滨,150040 |
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| 基金项目： | 黑龙江省自然科学基金
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黑龙江省研究生创新科研项目 |
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| 摘 要： | 采用免疫细胞化学法对H22细胞中的PI3K、AKT蛋白进行检测;分光光度法检测H22细胞中Caspase-3,9的活性对桦木酮酸通过抑制PI3K/AKT通路抗H22肝癌腹水瘤的机制进行初步研究.结果表明,桦木酮酸给药量为500 mg/（kg·d）和1000 mg/（kg·d）时,对H22腹水瘤有显著的抑制作用;当桦木酮酸给药量为1000 mg/（kg·d）时,PI3K和AKT蛋白的表达分别从56%和60%降到28%和31%;Caspase-3,9的活性在桦木酮酸给药量为500 mg/（kg·d）和1000 mg/（kg·d）时,与空白组相比均有显著性差异.说明桦木酮酸可能通过抑制PI3K/AKT细胞存活通路抑制细胞增殖,并通过提高Caspase-3,9的活性促进细胞凋亡而起到抗肿瘤的作用.
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| 关 键 词： | 桦木酮酸 PI3K AKT Caspase-3 9 |
| 文章编号： | 1672-0946(2008)03-0261-04 |
| 修稿时间： | 2007年10月12 |
Study of betulonic acid on anti-tumor by inhibiting PI3K/AKT pathways |
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| ZHANG Xiu-juan,HAN Lei,LING Li-li,LI Qiu-shi,JI Yu-bin,FANG Gui-zhen.Study of betulonic acid on anti-tumor by inhibiting PI3K/AKT pathways[J].Journal of Harbin University of Commerce :Natural Sciences Edition,2008,24(3):261-264. |
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| Authors: | ZHANG Xiu-juan HAN Lei LING Li-li LI Qiu-shi JI Yu-bin FANG Gui-zhen |
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| Institution: | ZHANG Xiu-juan, HAN Lei, LING Li-li ,LI Qiu-shi ,JI Yu-bin, FANG Gui-zhen( 1. Postdoctoral Research Station of Institute of Medicine of Center of Research and Development on Life and Environment Science, Harbin University of Commerce, Harbin 150076, China ;2. Engineering Research Center of Natural Anticancer Drugs, Ministry of Education, Harbin 150076, China; 3. College of Material and Engineering, Noethest Forestry University, Harbin 150040, China) |
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| Abstract: | To study the mechanism of betulonic acid on tumor bearing mice through inhibiting the PI3K, AKT. The immuocytochemistry method is used to determine the PI3K, AKT protein expression and the spectrophotometric method to detect the activity of caspase - 3,8 of tumor cells. The results showed that betulonic acid＇ s dose is 500 mg/（ kg · d） and 1 000 mg/（ kg · d） respectively, it have noticeable inhibition action oin tumor cells; when betulonic acid＇ s dose is 1 000 mg/（ kg · d）, the expression of PI3 K and AKT is decreased from 56% and 60% to 28% and 31%. When the betulonic acid＇ s dose is 500 mg/（kg· d） and 1 000 mg/（ kg·d） respectively, the caspase 3,9 activity have more significance difference than negative group. So the antitumor action of betulonic acid may be inducing apoptosis through inhibiting the PI3K, AKT pathways and promoting caspase - 3,9 activities. |
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| Keywords: | betulonic acid PI3 K AKT caspase - 3 9 |
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