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目的:探讨核仁素对心肌梗死后巨噬细胞极化的影响及其作用机制。方法:采用小鼠心肌梗死模型;采用心肌内注射核仁素RNA干扰的慢病毒载体,从整体水平观察核仁素低表达对小鼠心梗后死亡率的影响及对巨噬细胞极化的影响;采用流式细胞术检测巨噬细胞极化情况。结果:心肌梗死1 d后,核仁素表达减少,3 d后表达增加,5 d后明显升高,达(2.73±0.47)倍,7 d后有所下降。小鼠心肌梗死2 d、5 d后,心肌中巨噬细胞明显增多;心肌梗死2 d后心肌中M1型巨噬细胞占77.71%,而心肌梗死5 d后心肌中M2型巨噬细胞占82.13%。核仁素低表达可抑制心肌梗死5 d后M2型巨噬细胞的极化,但对巨噬细胞的侵润无明显影响,可明显减少心肌梗死后28 d的存活率。核仁素过表达可使巨噬细胞极化相关基因NOTCH1和STAT6的m RNA水平表达上调,而核仁素低表达可下调NOTCH1和STAT6的m RNA表达水平。结论:核仁素可调控心梗后巨噬细胞的极化,核仁素低表达可增加小鼠心梗后死亡率。
Objective: To investigate the effect of nucleolin on the polarization of macrophages after myocardial infarction and its mechanism. Methods: Myocardial infarction model was induced in mice. Lentiviral RNA interference lentiviral vectors were injected intramyocardially to observe the effect of low nuclein expression on post-MI mortality and macrophage polarization Effect; Detection of macrophage polarization using flow cytometry. Results: After 1 d of myocardial infarction, the expression of nucleolin decreased, and the expression increased 3 days later. The expression of nucleolin increased significantly after 5 days (2.73 ± 0.47) times and decreased after 7 days. Myocardial infarction in 2 d, 5 d after the macrophages in the myocardium increased significantly; 2 d after myocardial infarction myocardial M1 macrophages accounted for 77.71%, while 5 days after myocardial infarction in myocardial M2 macrophages accounted for 82.13 %. The low expression of nucleolin inhibits the polarization of M2 macrophages 5 d after myocardial infarction, but has no obvious effect on the infiltration of macrophages and can significantly reduce the survival rate of 28 d after myocardial infarction. Overexpression of nucleolin can up-regulate m RNA level of macrophage polarization-related genes NOTCH1 and STAT6, whereas low nucleolin expression down-regulates mRNA expression of NOTCH1 and STAT6. Conclusion: Nucleolin can regulate the polarization of macrophages after myocardial infarction. The low expression of nucleolin can increase the post-MI mortality in mice.