Effects of Curcumol on Apoptosis Induce Factor,Poly ADP-Ribose Polymerase and Caspase-3 in Lung Cancer Cell Line A549

CHEN Xu; WANG Juan; JIANG Xiao-shan; ZENG Jian-hong; HUNAG Feng-xiang

doi:CNKI:11-3495/R.20110809.1704.001

您当前的位置：

首页 >

文章列表页 >

Effects of Curcumol on Apoptosis Induce Factor,Poly ADP-Ribose Polymerase and Caspase-3 in Lung Cancer Cell Line A549

更新时间：2024-01-04

- Effects of Curcumol on Apoptosis Induce Factor,Poly ADP-Ribose Polymerase and Caspase-3 in Lung Cancer Cell Line A549
- Chinese Journal of Experimental Traditional Medical Formulae Vol. 17, Issue 19, Pages: 157-159(2011)
- 作者机构：
- 作者简介：
- 基金信息：
- DOI：CNKI:11-3495/R.20110809.1704.001
  CLC：
- Published：2011
- 稿件说明：
移动端阅览
CHEN Xu, WANG Juan, JIANG Xiao-shan, et al. Effects of Curcumol on Apoptosis Induce Factor,Poly ADP-Ribose Polymerase and Caspase-3 in Lung Cancer Cell Line A549[J]. Chinese journal of experimental traditional medical formulae, 2011, 17(19): 157-159.
DOI：

CHEN Xu, WANG Juan, JIANG Xiao-shan, et al. Effects of Curcumol on Apoptosis Induce Factor,Poly ADP-Ribose Polymerase and Caspase-3 in Lung Cancer Cell Line A549[J]. Chinese journal of experimental traditional medical formulae, 2011, 17(19): 157-159. DOI： CNKI:11-3495/R.20110809.1704.001.

摘要

目的: 观察莪术醇干预后

体外培养A549 细胞凋亡诱导因子(apoptosis induce factor

AIF)和聚ADP核糖聚合酶的表达情况

探讨莪术醇对非半胱天冬酶(caspase)依赖细胞凋亡的分子机制。方法: 以不同质量浓度的莪术醇(12.5

100 mg·L-1)及阴性组处理肺癌细胞

药物作用48 h后提取各组蛋白;采用Western blotting 法分别检测各组AIF

PARP

caspase-3蛋白表达

并进行统计学分析。结果: 经莪术醇处理后

阴性组的A549细胞的PARP相对蛋白表达量为0.545 3

AIF的相对蛋白表达量为0.358 6

而100 mg·L-1加药组的相对蛋白表达量分别为1.661 3和2.212 4

蛋白表达均随药物浓度的增加而增多

药物组与阴性组相比差异极显著(P<0.01)

而caspase-3的前体(32×103)表达受药物影响较小

其激活体(17×103)基本不表达。结论: 莪术醇可能主要是通过上调PARP蛋白的表达

进而将AIF转位到细胞核而引起凋亡的非依赖caspase途径来介导肺癌A549细胞的凋亡。

Abstract

Objective: To study the effects of curcumol on the expression of apoptosis induce factor(AIF)

poly ADP-ribose polymerase(PARP)and caspase-3 protein in lung cancer cell A549. Method: A549 cells were treated with different concentrations(0

12.5

100 mg·L-1)of curcumol for 48 hours

then the total protein was extracted from each group respectively. The expression of AIF

PARP and caspase-3 was detected by Western blotting. Result: The PARP and AIF protein expressions were significantly elevated in the treatment groups(1.661 3 and 2.212 4 respectively)compared with the model group(0.545 3 and 0.358 6 respectively)

in a dose dependent manner(P<0.01). The caspase-3 precursor(32×103)protein expression showed no significance difference among all the groups. Conclusion: Curcumol could induce apoptosis through caspase-independent pathway in human lung cancer cell A549

whose mechanism might be linked to up-regulation of the PARP protein and translocation of AIF.

关键词

Keywords

references

Views

下载量

CSCD

Alert me when the article has been cited

提交

Tools

Publicity Resources

Effect of Wenyang Sanjie Prescription on Tumor Inhibition and STAT3/HIF-1α Pathway in Lung Cancer Tumor-bearing Mice

Invasion and Metastasis Inhibition of Lung Cancer by Traditional Chinese Medicine： A Review

Mechanism of Traditional Chinese Medicine Regulating JAK/STAT Signaling Pathway to Intervene in Lung Cancer： A Review

Effect of Guiqi Yiyuan Ointment on Lewis Lung Cancer Mice by Increasing Autophagic Flux and Stabilizing PD-L1 Expression Through Regulation of ERK Signaling Pathway

Chinese Medicine Regulates Ferroptosis to Treat Lung Cancer： A Review

Related Author

WANG Xinxin

GUO Junhui

LI Honglin

ZHENG Fengyu

LI Jia

SUN Xu

ZHANG Lu

LIU Huaimin

Related Institution

Henan Province Hospital of Traditional Chinese Medicine

The Second Clinical Medical College， Henan University of Chinese Medicine

The Affiliated Cancer Hospital of Zhengzhou University/Henan Cancer Hospital

Henan Province Hospital of Traditional Chinese Medicine/The Second Affiliated Hospital of Henan University of Chinese Medicine

School of Basic Medicine， Gansu University of Chinese Medicine

AI问答

Postal code：100700
Tel：010-84076882 Email：syfjx_2010@188.com
Technical support is provided by Beijing Founder electronics co., LTD 京ICP备11006657号-10 京公网安备11010802024621
It is recommended to read the content of this site in Chrome&IE9+. Please switch to extreme mode in browser 360.
Cookies We use cookies to help provide and enhance our service and tailor content. By continuing, you agree to the use of cookies.

⁰