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Bim参与了Photofrin介导的光动力反应诱导细胞调亡

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 导读Bim(Bcl-2 interacting mediator of cell death)是新近发现的Bcl-2蛋白家族促凋亡成员之一。近期,光动力研究者发表论文称Bim参与了Photofrin介导的光动力反应诱导的细胞调亡,且认为增强Bim的活性可能成为抗肿瘤的一个潜在方向。

具体信息如下:


BACKGROUND/AIMS: 背景/目的

 

光动力疗法是一项前景广阔的非侵害性技术,已被成功的应用于人类肿瘤的治疗。研究表明Bcl-2家族蛋白在PDT诱导的细胞调亡中发挥了重要作用。然而,Bim是否参与了光动力治疗目前还不得而知。在这次的研究中,我们尝试确认Bim在Photofrin光动力治疗诱导人类肺腺癌ASTC-a-1细胞调亡中的作用。


 

Photodynamic therapy (PDT) is a promising noninvasive technique, which has been successfully applied to the treatment of human cancers.Studies have shown that the Bcl-2 family proteins play important roles in PDT-induced apoptosis. However, whether Bcl-2-interacting mediator of cell death (Bim) is involved in photodynamic treatment remains unknown. In this study, we attempt to determine the effect of Bim on Photofrin photodynamic treatment (PPT)-induced apoptosis in human lung adenocarcinoma ASTC-a-1 cells.


 

METHODS: 方法


用激光共聚焦扫描显微镜监测Bim/Bax细胞的迁移。用蛋白印记法测定了细胞中Bim蛋白和激活的caspase-3的水平。通过Caspase-3荧光底物分析测定了Caspase-3的活性。通过Hoechst33258染色和Pi染色以及流式细胞仪分析测定诱导的细胞调亡。用RNA干扰技术确定Bim在光动力治疗诱导的细胞调亡中的作用。


The translocation of Bim/Bax of the cells were monitored by laser confocal scanning microscope. The levels of Bim protein and activated caspase-3 in cells were detected by western blot assay. Caspase-3 activities were measured by Caspase-3 Fluorogenic Substrate (Ac-DEVD-AFC) analysis. The induction of apoptosis was detected by Hoechst 33258 and PI staining as well as flow cytometry analysis. The effect of Bim on PPT-induced apoptosis was determined by RNAi.



 

RESULTS: 结果


BimL移位到线粒体响应PPT,与下游的促调亡蛋白Bax活化作用相似。PPT增加了细胞中Bim和激活的Caspase-3的水平并且通过RNA干扰技术降低Bim的表达从而大大的免受了Caspase-3的活性(干扰)。在shRNA-Bim 转染的细胞中PPT 诱导的细胞调亡被抑制了。


BimL translocated to mitochondria in response to PPT, similar to the downstream pro-apoptotic protein Bax activation. PPT increased the level of Bim and activated caspase-3 in cells and that knockdown of Bim by RNAi significantly protected against caspase-3 activity. PPT-induced apoptosis were suppressed in cells transfected with shRNA-Bim.

 

CONCLUSION: 结论


我们证明了Bim参与了PPT-诱导人类ASTC-a-1肺腺癌细胞的细胞调亡以及建议增强Bim的活性可能是治疗人类肿瘤的一个潜在的策略。


We demonstrated the involvement of Bim in PPT-induced apoptosis in human ASTC-a-1 lung adenocarcinoma cells and suggested that enhancing Bim activity might be a potential strategy for treating human cancers.


文章来源:

 

Cell Physiol Biochem. 2015;35(4):1527-36. 

Involvement of Bim in Photofrin-mediated photodynamically induced apoptosis.

Wang X1, He X, Hu S, Sun A, Lu C.

1Laboratory of Neuronal Network and Brain Diseases Modulation, School of Medicine, Yangtze University, Jingzhou, China.

神经元网络和脑部疾病调制实验室,长江大学医学院,荆州,中国
 

原文链接:http://www.ncbi.nlm.nih.gov/pubmed/?term=Involvement+of+Bim+in+Photofrin-mediated+photodynamically+induced+apoptosis.


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