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研究巨噬细胞移动抑制因子(macrophage migration inhibitory factor,MIF)缺失对皮下注射苯肾上腺素(phenylephrine,PE)诱导的小鼠心肌肥厚的影响.利用MIF敲除(MIFknockout,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超检测到小鼠心脏结构功能的改变.末端脱氧核苷酸转移酶介导的d UTP缺节末端标记(terminal deoxynucleotidyl transferase(Td T)-mediated d UTP nick end labeling,TUNEL)法检测到小鼠心肌细胞凋亡.分别用实时定量逆转录多聚酶链反应(quantitative reverse-transcription-polymerase chain reaction,q RT-PCR)和Western Blot方法检测SOD1,SOD2和Trx2的表达.1连续3 d 20 mg/(kg·d)皮下注射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;2 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;3注射PE诱导MIF-KO小鼠心肌中SOD1和Trx2表达水平降低,而且MIF-KO小鼠心肌中Trx2表达水平显著低于野生型对照小鼠.MIF缺失会降低SOD1和Trx2的表达水平,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.
To investigate the effect of macrophage migration inhibitory factor (MIF) deletion on myocardial hypertrophy induced by subcutaneous injection of phenylephrine (PE) in mice.MIF knockout (MIF-KO) mice and Its wild-type control mice were established subcutaneous injection of PE-induced mouse model of cardiac hypertrophy.Mouse heart B-test detected structural changes in cardiac function in mice.Delta terminal deoxynucleotidyl transferase-mediated dUTP missing ends (TdT) -mediated dUTP nick end labeling (TUNEL) method was used to detect the cardiomyocyte apoptosis in mice.Quantitative reverse-transcription-polymerase chain reaction (q RT -PCR) and Western Blot method were used to detect the expression of SOD1, SOD2 and Trx2.1 PE induced cardiac hypertrophy in mice subcutaneously injected with 20 mg / (kg · d) for 3 d, PE induced MIF-KO induced cardiac hypertrophy 2 TUNEL results showed that the PE induced MIF-KO mice myocardial apoptosis than the wild-type control mice; 3 PE-induced MIF-KO mice The expression of Trx2 in myocardium of MIF-KO mice was significantly lower than that of wild-type control mice.MIF deficiency decreased the expression of SOD1 and Trx2, which in turn increased the expression of phenylephrine-induced mouse myocardium Apoptosis and cardiac hypertrophy.