Relationship between macrophage infiltration in the coronary plaque and downstream myocardial perfusion in mice
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目的 探究小鼠冠状动脉斑块内巨噬细胞浸润程度与其下游心肌灌注的关系。 方法 实验组采用ApoE基因敲除联合高脂喂养的方法建立冠状动脉斑块小鼠模型20只，对照组选用性别和年龄相匹配的具有相同遗传背景的C57BL/6小鼠20只。对所有实验动物行心肌造影超声心动图联合腺苷负荷试验测量静息及负荷状态下小鼠左心室心肌前间隔和后壁的A值、β值以及A×β值。采用酶联免疫吸附试验方法检测血清白细胞介素6(IL-6)和肿瘤坏死因子α(TNF-α)水平，通过病理免疫组化染色评估冠状动脉斑块内巨噬细胞浸润程度，并与上述指标做相关性分析。 结果 对照组与实验组的心率、左心室结构参数比较，差异无统计学意义(均P>0.05)。实验组的左心室射血分数较对照组显著降低(P＝0.021)，而体重、血清三酰甘油、总胆固醇、高密度脂蛋白胆固醇、低密度脂蛋白胆固醇、IL-6及TNF-α水平较对照组显著升高(均P<0.05)。腺苷负荷状态下，实验组左心室心肌前间隔和后壁的A值、β值、A×β值显著低于对照组(均P<0.05)。在实验组中，左冠状动脉主干斑块内巨噬细胞浸润率与血清TNF-α水平呈显著正相关(r＝0.63，P＝0.003)，而与腺苷负荷状态下左心室前间隔及后壁心肌造影A×β值呈显著负相关(r＝－0.74，P<0.001；r＝－0.72，P<0.001)。 结论 ApoE基因敲除小鼠冠状动脉粥样硬化模型的下游心肌灌注与其冠状动脉斑块中巨噬细胞的浸润程度有关，巨噬细胞可能通过释放炎症介质TNF-α发挥作用。 Objective To explore the relationship between macrophage infiltration in the coronary plaque and downstream myocardial perfusion in mice. Methods The experimental group consisted of 20 ApoE knockout mice models of the coronary plaque established by feeding with cholesterol-rich diets, and the control group consisted of 20 sex- and age-matched C57BL/6 mice with the same genetic background as ApoE mice.Adenosine stress myocardial contrast echocardiography was performed on all experimental animals to obtain the values of A, β and A×β of the left ventricular myocardium in anteroseptal and posterior walls both in the resting status and during adenosine stress. Concentrations of serum interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) were determined using mouse enzyme-linked immunosorbent assay kits according to the manufacturer′s instructions. The degree of macrophage infiltration in the coronary plaque was evaluated by pathological immunohistochemistry staining and the correlations with the above indicators were analyzed. Results There were no statistically significant differences in heart rate and left ventricular structural parameters between two groups (all P>0.05). The experimental group had a lower left ventricular ejection fraction(P=0.021), and higher weight and serum levels of triglycerides, total cholesterol, high-density lipoprotein, low-density lipoprotein, IL-6, and TNF-α than the control group (allP<0.05). The values of A, β and A × β of the left ventricular myocardium in anteroseptal and posterior walls in the experimental group were significantly lower than those in the control group during adenosine stress (allP<0.05). In the experimental group, the value of the macrophage infiltration found in the plaque of the left main coronary artery correlated positively with the level of serum TNF-α (r=0.63, P=0.003) and negatively correlated with the values of A×β of the left ventricular myocardium in anteroseptal and posterior walls during adenosine stress (r=-0.74, P<0.001 r=-0.72, P<0.001 respectively). Conclusions Myocardial perfusion in ApoE knockout mice models of the coronary atherosclerosis was related with degree of macrophage infiltration in the coronary plaque, and macrophages may play a role by releasing inflammatory mediator TNF-α.
Objective To explore the relationship between macrophage infiltration in the coronary plaque and downstream myocardial perfusion in mice. Methods The experimental group consisted of 20 ApoE knockout mice models of the coronary plaque established by feeding with cholesterol-rich diets, and the control group consisted of 20 sex- and age-matched C57BL/6 mice with the same genetic background as ApoE mice.Adenosine stress myocardial contrast echocardiography was performed on all experimental animals to obtain the values of A, β and A×β of the left ventricular myocardium in anteroseptal and posterior walls both in the resting status and during adenosine stress. Concentrations of serum interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) were determined using mouse enzyme-linked immunosorbent assay kits according to the manufacturer′s instructions. The degree of macrophage infiltration in the coronary plaque was evaluated by pathological immunohistochemistry staining and the correlations with the above indicators were analyzed. Results There were no statistically significant differences in heart rate and left ventricular structural parameters between two groups (all P>0.05). The experimental group had a lower left ventricular ejection fraction(P=0.021), and higher weight and serum levels of triglycerides, total cholesterol, high-density lipoprotein, low-density lipoprotein, IL-6, and TNF-α than the control group (allP<0.05). The values of A, β and A × β of the left ventricular myocardium in anteroseptal and posterior walls in the experimental group were significantly lower than those in the control group during adenosine stress (allP<0.05). In the experimental group, the value of the macrophage infiltration found in the plaque of the left main coronary artery correlated positively with the level of serum TNF-α (r=0.63, P=0.003) and negatively correlated with the values of A×β of the left ventricular myocardium in anteroseptal and posterior walls during adenosine stress (r=-0.74, P<0.001 r=-0.72, P<0.001 respectively). Conclusions Myocardial perfusion in ApoE knockout mice models of the coronary atherosclerosis was related with degree of macrophage infiltration in the coronary plaque, and macrophages may play a role by releasing inflammatory mediator TNF-α.
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