论文部分内容阅读
目的:探讨经IFN-γ刺激后,人外周血单个核细胞OX40L表达的变化,以及辛伐他汀对单个核细胞OX40L表达的影响。方法:将实验标本随机分为2组,分别干扰素-γ(IFN-γ)刺激组、辛伐他汀干预组。应用RT-PCR及Western blotting技术,观察IFN-γ诱导的人外周血单个核细胞OX40L表达情况及辛伐他汀对人单个核细胞OX40L表达的影响。结果:1.1000 U/ml IFN-与人单个核细胞共同培养24h后,OX40L mRNA和蛋白水平的表达明显增加。2.预先给予10 mol/L的辛伐他汀干预1h可以明显降低IFN-诱导的OX40L表达。结论:IFN-可诱导人单个核细胞OX40L表达。辛伐他汀可以抑制IFN-诱导人单个核细胞OX40L表达的增强,从而可能抑制了OX40L信号通路介导的与炎症有关的血管损伤,延缓动脉粥样硬化的进程。
Objective: To investigate the changes of OX40L expression in human peripheral blood mononuclear cells stimulated by IFN-γ and the effect of simvastatin on the expression of OX40L in mononuclear cells. Methods: The experimental specimens were randomly divided into two groups, respectively interferon-γ (IFN-γ) stimulation group, simvastatin intervention group. The expression of OX40L in human peripheral blood mononuclear cells induced by IFN-γ and the effect of simvastatin on the expression of OX40L in human mononuclear cells were observed by RT-PCR and Western blotting. Results: OX40L mRNA and protein levels were significantly increased after co-cultured with 1.1000 U / ml IFN-γ and human mononuclear cells for 24 h. Pretreatment with 10 mol / L simvastatin for 1 h significantly reduced IFN-induced OX40L expression. Conclusion: IFN-induced OX40L expression in human mononuclear cells. Simvastatin can inhibit the IFN-induced OX40L expression in human mononuclear cells, which may inhibit the OX40L signaling-mediated inflammation-related vascular injury, slowing the process of atherosclerosis.