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首页> 外文期刊>Journal of Traditional Chinese Medical Sciences >Inductive effect of hydroxyl safflower yellow-A on apoptosis in abnormal HUVEC via the mitochondrial pathway
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Inductive effect of hydroxyl safflower yellow-A on apoptosis in abnormal HUVEC via the mitochondrial pathway

机译:羟基红花黄A通过线粒体途径诱导HUVEC异常凋亡的诱导作用

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摘要

Objective To investigate the mechanism by which hydroxyl safflower yellow A, an active component of safflower ( Carthamus tinctorius L.), promotes apoptosis in abnormal human umbilical vein endothelial cells (HUVECs). Methods Supernatant of BGC-823 was used to stimulate HUVECs to establish a model of abnormal proliferation of HUVECs. After determining an ideal concentration of HSYA by MTT assay, apoptosis was detected with flow cytometry and TUNEL assay. Mechanism of apoptosis was assessed using quantitative real-time polymerase chain reaction, Western blot, and ELISA. Results A range of concentrations of HSYA inhibited proliferation and promoted apoptosis of abnormal HUVECs. As the rate of apoptosis increased, mRNA expression of caspase-3 increased while expression of mutant p53 decreased. HSYA had no effect on Fas gene expression. Analogously, protein expression of Bax was increased while those of Bcl-2, Fas, and Fas-L were decreased. Conclusions HSYA appears to induce apoptosis of HUVECs with the stimulation of the supernatant of tumor cells. The mechanism of apoptosis by HSYA may involve activation of the mitochondrial apoptotic pathway and regulation of the expressions of Bcl-2, Bax, and p53.
机译:目的研究红花的活性成分羟基红花黄A(Carthhams tinctorius L.)促进异常人脐静脉内皮细胞(HUVEC)凋亡的机制。方法采用BGC-823上清液刺激HUVECs,建立HUVECs异常增殖模型。通过MTT测定确定理想的HSYA浓度后,通过流式细胞仪和TUNEL测定检测细胞凋亡。使用定量实时聚合酶链反应,蛋白质印迹和ELISA评估凋亡的机制。结果一定浓度的HSYA抑制异常HUVECs的增殖并促进其凋亡。随着凋亡率的增加,caspase-3 mRNA的表达增加,而突变型p53的表达减少。 HSYA对Fas基因表达没有影响。类似地,Bax的蛋白质表达增加,而Bcl-2,Fas和Fas-L的蛋白质表达减少。结论HSYA可能通过刺激肿瘤细胞上清液诱导HUVEC凋亡。 HSYA引起的凋亡机制可能涉及线粒体凋亡途径的激活和Bcl-2,Bax和p53表达的调节。

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