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作 者:柴晓宇[1] 许慧莹[1] 刘钟桧 易亮[1] 刘新民[1]
出 处:《现代生物医学进展》2017年第15期2801-2804,共4页Progress in Modern Biomedicine
基 金:国家自然科学基金项目(81270114)
摘 要:目的:探究氯化钴对于原代大鼠肺动脉成纤维细胞(PAF)的增殖、迁移、表型转化作用的影响。方法:分离培养大鼠肺动脉成纤维细胞,利用氯化钴刺激PAF细胞,并通过MTT、细胞划痕、Transwell、表型转化标志蛋白测定以及PI3K/Akt信号通路蛋白的变化研究氯化钴对PAF的影响。结果:MTT结果显示,与对照组相比,氯化钴可以抑制大鼠肺动脉成纤维细胞的增殖活性(P<0.001),并呈浓度依赖性。划痕实验及Transwell实验提示较高氯化钴(200μmol·L^(-1))处理PAF细胞后可以抑制细胞迁移。随浓度增加,氯化钴可以抑制PAF的P110α、p-Akt蛋白表达。结论:氯化钴对于体外培养的原代大鼠肺动脉成纤维细胞的增殖、迁移和表型转化特性有一定的抑制作用,这可能与氯化钴抑制PI3K/Akt信号通路的表达有关。Objective:Study the effects of cobalt chloride on the proliferation,migration and phenotype transformation on the primary pulmonary artery fibroblasts (PAF) from rat.Methods:Using cobalt chloride to stimulate the established PAF.Value the effects of cobalt chloride on PAF by MTT,cell scratch,Transwell,phenotype marker protein expression and PI3K/Akt signaling pathway proteins expressions.Results:Compared with the control group,MTT results showed that cobalt chloride could decrease the proliferation activity of PAF in a concentration-dependent manner.Scratch and Transwell assays showed that higher concentrations of cobalt chloride could inhibit the migration of PAF.Cobalt chloride could decrease the protein expressions of P110α and p-Akt in a concentration-dependent manner.Conclusions:Cobalt chloride could inhibit the proliferation,migration and phenotype conversion characteristics of PAF by affecting the expression of PI3K/Akt signaling pathway which might involve in the regulation of cell behaviors.
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