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目的:研究巨噬细胞移动抑制因子(MIF)缺失对皮下注射苯肾上腺素(PE)诱导的小鼠心肌肥厚的影响。方法:利用MIF敲除(MIF-KO)小鼠及其野生型对照小鼠,分别建立皮下注射PE诱导的小鼠心肌肥厚模型。小动物心脏B超检测小鼠心脏的结构功能改变。末端脱氧核苷酸转移酶介导的d UTP缺口末端标记(TUNEL)法检测小鼠心肌细胞凋亡。分别用荧光定量PCR和Western blot方法分别检测SOD1、SOD2和Trx2的表达。结果:连续3 d皮下注射20 mg·kg~(-1)·d~(-1)PE可诱导小鼠发生心肌肥厚,注射PE诱导MIF-KO小鼠发生心肌肥厚的程度高于野生型对照小鼠。TUNEL结果显示,注射PE诱导MIF-KO小鼠心肌发生凋亡的程度高于野生型对照小鼠。注射PE诱导MIF-KO小鼠心肌中SOD1和Trx2表达降低,而且MIF-KO小鼠心肌中Trx2水平显著低于野生型对照小鼠。结论:MIF缺失降低SOD1和Trx2表达,进而加重苯肾上腺素诱导的小鼠心肌细胞凋亡和心肌肥厚。
AIM: To investigate the effect of macrophage migration inhibitory factor (MIF) on cardiac hypertrophy in mice induced by phenylephrine (PE) injected subcutaneously. Methods: MIF-knockout (MIF-KO) mice and their wild-type control mice were used to establish model of cardiac hypertrophy induced by PE in mice. Changes of structural function of heart in mice by B-mode ultrasonography. Terminal deoxynucleotidyl transferase - mediated dUTP nick end labeling (TUNEL) assay was used to detect cardiomyocyte apoptosis in mice. The expression of SOD1, SOD2 and Trx2 were detected by fluorescence quantitative PCR and Western blot respectively. Results: Cardiac hypertrophy was induced in mice by subcutaneous injection of 20 mg · kg -1 d -1 PE for 3 days, and the degree of myocardial hypertrophy induced by PE in MIF-KO mice was higher than that of wild-type control Mouse. The results of TUNEL showed that the PE-induced apoptosis in myocardium of MIF-KO mice was higher than that of wild-type control mice. Injection of PE induced a decrease in the expression of SOD1 and Trx2 in the myocardium of MIF-KO mice, and the level of Trx2 in myocardium of MIF-KO mice was significantly lower than that in wild-type control mice. CONCLUSION: MIF deletion reduces the expression of SOD1 and Trx2, which further aggravates phenylephrine-induced cardiomyocyte apoptosis and cardiac hypertrophy in mice.