华蟾素抗肺癌细胞的实验研究

摘要

目的：探究华蟾素的抗肺癌活性。方法培养肺癌 A549细胞,对华蟾素、环孢素-A(CsA)、萨菲菌素 A(SfA)作用于肺癌 A549细胞后的细胞存活率、细胞死亡率、细胞凋亡率以及线粒体膜电位(MMP)进行检测；建立小鼠移植瘤模型,对华蟾素作用于小鼠移植瘤模型后的肿瘤体积以及小鼠存活率进行检测,并整理数据进行统计学对比分析。结果通过小鼠移植瘤模型,该研究发现华蟾素抑制了 A549肺癌细胞在体内生长。研究结果表明亲环蛋白 D(Cyp-D)依赖的线粒体通透性转换孔(mPTP)开放可调节由华蟾素诱导的肺癌细胞的非凋亡性死亡。Cyp-D 的抑制剂环孢素-A(CsA),mPTP 的阻断剂萨菲菌素 A(SfA)极明显地阻碍了由华蟾素诱导的线粒体膜电位(MMP)的下降和 A549细胞的死亡(非凋亡)。结论华蟾素可以诱导肺癌细胞死亡,值得进一步研究,有望成为一种新型的抗肺癌药物。%Objective Explore the potential of Huachan element resistance to lung cancer.Methods Cultivate the A549 lung cancer cells.After HuaChan element and cyclosporine A(CsA),safi rhzomorph A (SfA)role in the A549 lung cancer cells,testing cell survival and cell death,cell apoptosis rate and mitochondrial membrane potential (MMP).Establish the mice transplanted tumor model,After HuaChan element role in the mice transplanted tumor model,testing the tumor volume and the survival rate of mice.And collates data for statistical analysis.Results By mice transplanted tumor model,Data show that cyclophilin D (Cyp,cyclophilin D-D)rely on mitochondrial permeabil-ity transition pore (mitochondrial permeability transition pore,mPTP)open the adjustable by Huachan induced lung cancer non apoptotic cell death.Cyp inhibitors-D part of spore element-A (cyclosporine A,CsA),the blocker mPTP safi rhzomorph A (sanglifehrin A,SfA)extremely significantly hindered by Huachan induced mitochondrial mem-brane potential (mitochondrial membranepotential,MMPs)fall and A549 cell death (apoptosis).Conclusion The study found that Huachan inhibit the growth of the A549 lung cancer cells in the body.Research results show that HuaChan element is worth further study,as a new type of lung cancer drug resistance.