2β, 3β, 23-trihydroxy-urs-12-ene-28-olic acid (TUA) isolated from Actinidia chinensis Radix inhibits NCI-H460 cell proliferation by decreasing NF-κB expression
2β, 3β, 23-trihydroxy-urs-12-ene-28-olic acid (TUA) isolated from Actinidia chinensis Radix inhibits NCI-H460 cell proliferation by decreasing NF-κB expression
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从猕猴桃中分离的 2β, 3β, 23-三羟基-urs-12-ene-28-olic Acid (TUA) Radix 通过降低 NF-kappa B 表达来抑制 NCI-H460 细胞增殖
DOI：
10.1016/j.cbi.2015.06.038
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发表时间：
2015-10-05
影响因子：
5.1
通讯作者：
Liu, Ta-Si
中科院分区：
文献类型：
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作者：
Cheng, Qi-Lai;Li, Hong-Liang;Liu, Ta-Si
从猕猴桃（A. chinensis Radix）的根中分离得到了一种天然熊果酸化合物2 β， 3 β， 23-三羟基脲-12-烯-28-果酸（TUA）。由于大量的三萜化合物在体外对多种类型的癌细胞都有明显的抗癌作用，本研究探讨了TUA对非小细胞肺癌细胞（nsclc）的抗癌作用，并在NCI-H460细胞系中探讨了TUA的潜在凋亡机制。分别采用细胞计数试剂盒-8 （CCK-8）法和流式细胞术检测细胞增殖、细胞凋亡和细胞周期。用EMSA法测定转录因子nf - κ B的活性。western blotting检测细胞凋亡和增殖相关蛋白的表达。RT-PCR检测TUA对NCI-H460细胞NF-kappa B mRNA表达的影响。TUA显著抑制NCI-H460细胞活力。此外，通过细胞周期分析，TUA在NCI-H460细胞中以浓度依赖的方式显著增加了亚G1群体。这种作用伴随着p65 （NF-kappa B亚基）通过抑制I kappa B α磷酸化和抑制p65 mRNA表达而失活。总的来说，我们的研究结果表明，TUA通过抑制NCI-H460细胞中NF-kappa B （p65）的表达水平和激活I kappa B α来诱导细胞凋亡，作为肺癌治疗的有效抗癌候选药物。(C) 2015年由爱思唯尔爱尔兰有限公司出版。
A natural ursolic compound, 2 beta, 3 beta, 23-trihydroxy-urs-12-ene-28-olic acid (TUA) was isolated from the root of Actinidia chinensis Planch (A. chinensis Radix). Since a large number of triterpenoid compound has marked anticancer effects toward various types of cancer cell lines in vitro, this study was carried out to investigate the anticancer effect of TUA in non-small cell lung cancer cells (NSCLCCs) and the underlying apoptotic mechanism of TUA was examined in NCI-H460 cell lines. Cell proliferation, apoptosis and cell cycle were measured using a cell counting kit-8 (CCK-8) assay and flow cytometry, respectively. The activity of transcription factor NF-kappa B was determined by EMSA method. The expression of apoptosis- and proliferation-related proteins was determined by western blotting. The effect of TUA on NF-kappa B mRNA expression in NCI-H460 cells was detected by RT-PCR. TUA significantly suppressed the viability of NCI-H460 cells. Also, TUA significantly increased the sub G1 population by cell cycle analysis and in a concentration dependent manner in NCI-H460 cells. Such an effect was accompanied by p65 (NF-kappa B subunit) inactivation by an inhibition of I kappa B alpha phosphorylation, and by inhibition of p65 mRNA expressions. Consistently Overall, our findings suggest that TUA induces apoptosis via inhibition of NF-kappa B (p65) expression level and activation of I kappa B alpha in NCI-H460 cells as a potent anticancer candidate for lung cancer treatment. (C) 2015 Published by Elsevier Ireland Ltd.