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PPARγ激活在蛇葡萄素抑制乳腺癌细胞增殖和诱导凋亡中的作用
Role of PPARγ activation in cell growth inhibition and apoptosis inducement by ampelopsin in breast cancer cells
- 第三军医大学学报 2018年40卷第13期 页码：1185-1191
- 作者机构：
1.401320 重庆，重庆市巴南区人民医院临床营养科
2.400038 重庆，陆军军医大学(第三军医大学)军事预防医学系营养与食品卫生学教研室
- 作者简介：
[周永，E-mail:zhouyong0305@126.com ZHOU Yong, E-mail: zhouyong0305@126.com
- 基金信息：重庆市基础科学与前沿技术研究项目(CSTC2017jcyjAX0305);陆军军医大学电磁辐射医学防护教育部重点实验室开放课题(2017DCKF002)
DOI：10.16016/j.1000-5404.201712210
中图分类号： R151.3;R730.23;R737.9收稿：2017-12-22，
修回：2018-01-25，
纸质出版：2018-07-15
- 稿件说明：
移动端阅览
周永, 郑金英, 金小玲, 等. PPARγ激活在蛇葡萄素抑制乳腺癌细胞增殖和诱导凋亡中的作用[J]. 第三军医大学学报, 2018,40(13):1185-1191.
Yong ZHOU, Jinying ZHENG, Xiaoling JIN, et al. Role of PPARγ activation in cell growth inhibition and apoptosis inducement by ampelopsin in breast cancer cells[J]. Journal of Third Military Medical University, 2018, 40(13): 1185-1191.
周永, 郑金英, 金小玲, 等. PPARγ激活在蛇葡萄素抑制乳腺癌细胞增殖和诱导凋亡中的作用[J]. 第三军医大学学报, 2018,40(13):1185-1191. DOI： 10.16016/j.1000-5404.201712210.
Yong ZHOU, Jinying ZHENG, Xiaoling JIN, et al. Role of PPARγ activation in cell growth inhibition and apoptosis inducement by ampelopsin in breast cancer cells[J]. Journal of Third Military Medical University, 2018, 40(13): 1185-1191. DOI： 10.16016/j.1000-5404.201712210.
摘要
目的
2
探讨过氧化物酶体增殖激活物受体γ(peroxisome proliferators-activated receptorγ
PPARγ)的激活在蛇葡萄素(ampelopsin
AMP)抑制乳腺癌细胞增殖和诱导细胞增殖凋亡中的作用。
方法
2
以不同浓度AMP(20、40、60、80 μmol/L)分别处理人乳腺癌MDA-MB-231、MCF-7细胞24 h后，荧光素酶报告基因法检测AMP对PPARγ的激活作用，CCK-8检测细胞活力，流式细胞仪检测细胞凋亡，Western blot检测凋亡相关蛋白的表达，Caspase-3活性检测试剂盒检测Caspase-3活性。
结果
2
与PPARγ激动剂罗格列酮一样，AMP剂量依赖性地增强报告基因荧光素酶活性，同时显著抑制乳腺癌细胞增殖并诱导细胞凋亡(
P
＜0.05)；Western blot检测结果显示，AMP在显著上调乳腺癌细胞凋亡相关蛋白Bax、PTEN、活化Caspase-3表达的同时下调Bcl-2蛋白及Bcl-2/Bax比值；激酶活性检测结果显示，AMP可显著增强Caspase-3激酶活性，以上作用均可被PPARγ特异性拮抗剂GW9662显著削弱。
结论
2
AMP可能是PPARγ的天然激动剂，其通过激活PPARγ信号途径抑制乳腺癌细胞增殖并诱导细胞凋亡。
Abstract
Objective
2
To investigate whether the activation of proliferators-activated receptor γ (PPARγ) is required for ampelopsin (AMP)-induced cell growth inhibition and apoptosis in human breast cancer cells.
Methods
2
After different concentrations of AMP (20
40
60 and 80 μmol/L) was used to treat breast cancer cell lines MCF-7 and MDA-MB-231 for 24 h respectively
PPARγ activity was measured by luciferase reporter assay
cell viability was assessed by CCK-8 assay
and cell apoptosis was measured by flow cytometry with Annexin V-FITC/PI staining. Western blotting was used to measure the expression of apoptosis related proteins
and a clorimetric assay kit was employed to detect Caspase-3 activity.
Results
2
As PPARγ agonist rosiglitazone
AMP treatment also enhanced the activity of luciferase rep
orter
inhibited cell viability and induced apoptosis (
P
<
0.05) in MCF-7 and MDA-MB-231 cells in dose-dependent manners. Furthermore
Western blotting showed that AMP significantly up-regulated apoptosis related proteins Bax and PTEN
activated Caspase-3
down-regulated Bcl-2 and decreased the ratio of Bcl-2/Bax. Clorimetric assay indicated that the treatment enhanced the activity of Caspase-3. All above results could be obviously attenuated by PPARγ specific antagonist GW9662.
Conclusion
2
AMP maybe a natural agonist of PPARγ
and it can suppress cell proliferation and induce apoptosis in breast cancer cells by activating PPARγ.
关键词
Keywords
references
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