首页|松萝酸抑制人膀胱癌细胞增殖作用机制研究

松萝酸抑制人膀胱癌细胞增殖作用机制研究

Inhibitory Effect of Usnic Acid on Proliferation of Human Bladder Cancer Cells

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为了探究松萝酸对人膀胱癌的影响,体外培养人膀胱癌细胞T24、RT4,用不同浓度(12.5、25、50、100、200μmol/L)的松萝酸分别处理T24、RT4细胞24 h和48 h,采用MTT法检测T24、RT4细胞的增殖情况.研究结果发现松萝酸处理后细胞内的活性氧(ROS)水平增加且通过线粒体途径、死亡受体途径来诱导T24细胞发生凋亡:(1)松萝酸对T24、RT4细胞增殖均有抑制作用,且均呈现时间和剂量依赖性,其中,松萝酸对T24细胞增殖的抑制率更高;(2)通过Hoechst 33342染色与Annexin V-FITC/PI双染发现,随着松萝酸浓度的升高,凋亡的T24细胞逐渐增多;(3)T24 细胞经松萝酸处理后,细胞内 ROS 水平升高,cleaved-Caspase-3、cleaved-Caspase-8、cleaved-Caspase-9 和 Bax蛋白的表达量增加,Caspase-3、Caspase-8、Caspase-9和Bcl-2蛋白的表达量降低,且Bax蛋白表达量与Bel-2蛋白表达量的比值增加.
In order to investigate the effect of usnic acid on human bladder cancer,cultured human bladder cancer cells T24 and RT4 were treated with different concentrations of usnic acid(12.5,25,50,100,200 μmol/L)for 24 h and 48 h,respectively,and the proliferation of T24 and RT4 cells was detected by MTT assay.The re-sults showed that intracellular reactive oxygen species(ROS)levels were increased after treatment with usnic acid,and apoptosis of T24 cells was induced through mitochondrial pathway and death receptor pathway:(1)Usnic acid inhibited the proliferation of T24 and RT4 cells in a time-dependent and dose-dependent manner,and the inhibitory rate of usnic acid on T24 cell proliferation was higher.(2)By Hoechst 33342 staining and An-nexin V-FITC/PI double staining,apoptotic T24 cells gradually increased with the increase of the concentration of usnic acid.(3)After treatment with usnic acid,the level of intracellular ROS increased,the expression of Bax,cleaved-Caspase-8,cleaved-Caspase-9 and cleaved-Caspase-3 protein increased,the expression of Bcl-2,Caspase-3,Caspase-8 and caspase-9 decreased,and the ratio of Bax protein expression to Bcl-2 pro-tein expression increased.

usnic acidbladder cancerapoptosismitochondrial pathwaydeath receptor pathway

曹鹤、史丽颖、郭秀磊、于大永

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大连大学生命科学与技术学院,大连 116622

松萝酸 膀胱癌 凋亡 线粒体途径 死亡受体途径

辽宁省科学技术计划项目

2019-ZD-0564

2024

华南师范大学学报(自然科学版)
华南师范大学

华南师范大学学报(自然科学版)

CSTPCD北大核心
影响因子:0.413
ISSN:1000-5463
年,卷(期):2024.56(1)
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