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目的:探讨吡格列酮是否具有改善斑块易损性,降低易损斑块的破裂率的作用及其可能机制。方法:将20只家兔随机分为两组:药物干预组(n=10),对照组(n=10)。采用间断高脂饲养方法制造动脉粥样硬化模型,并进行斑块破裂激发试验。药物干预组于第1~18周在原饲料里添加吡格列酮(10 mg獉kg-1獉d-1)。于实验初期、中期、晚期分别留取血液标本进行MMP-9浓度测定。斑块破裂激发试验后处死动物,留取主动脉标本进行HE染色、巨噬细胞RAM-11及新生血管CD-31免疫组化染色,使用NIS-Elements AR Analysis病理图像分析系统分析斑块形态,测定斑块面积,进行巨噬细胞、新生血管计数。结果:实验中期及晚期,药物干预组血清(MMP-9)浓度均较对照组低[(2.25±0.11)vs.(2.60±0.19),P=0.040;(2.27±1.17)vs.(2.70±0.37),P=0.010]。实验晚期,药物干预组血清MMP-9浓度较对照组低[(2.27±1.17)vs.(2.70±0.37),P=0.010]。斑块破裂激发试验后,药物干预组组血栓形成率较对照组明显减少(14.62%vs.39.07%,P=0.000)。与对照组相比,药物干预组斑块面积小[(0.029±0.018)vs.(0.186±0.093),P=0.033]、巨噬细胞浸润少[(8.800±3.936)vs.(30.130±4.188),P=0.003]、新生血管数量少[(80.267±13.094)vs.(162.637±73.112),P=0.022]。结论:吡格列酮通过降低斑块内炎症程度提高斑块的稳定性,降低易损斑块的破裂率。
Objective: To investigate whether pioglitazone can improve plaque vulnerability and reduce the rate of rupture of vulnerable plaque and its possible mechanism. Methods: Twenty rabbits were randomly divided into two groups: drug intervention group (n = 10) and control group (n = 10). Atherosclerosis model was made by intermittent high-fat feeding method, and plaque rupture provocation test was carried out. Drug intervention group pioglitazone (10 mg 獉 kg-1 獉 d-1) was added to the original feed from the first week to the 18th week. Blood samples were collected at the beginning, middle and late stages of the experiment to determine the concentration of MMP-9. Plaque rupture challenge test animals were sacrificed, aortic specimens were taken for HE staining, macrophages RAM-11 and angiogenesis CD-31 immunohistochemical staining, using NIS-Elements AR Analysis pathological image analysis system analysis of plaque morphology, Plaque area determination, macrophages, neovascular count. Results: The serum levels of MMP-9 in the intervention group were lower than those in the control group at the middle and late stages of the experiment (2.25 ± 0.11 vs. 2.60 ± 0.19, P = 0.040, 2.27 ± 1.17 vs. 2.70 ± 0.37), P = 0.010]. At the end of the experiment, serum MMP-9 concentration in the intervention group was lower than that in the control group [(2.27 ± 1.17) vs. (2.70 ± 0.37), P = 0.010]. After the plaque rupture provocation test, the thrombosis rate in the intervention group was significantly lower than that in the control group (14.62% vs.39.07%, P = 0.000). Compared with the control group, the area of plaque in the intervention group was smaller than that of the control group [(0.029 ± 0.018) vs. (0.186 ± 0.093), P = 0.033], less macrophage infiltration [(8.800 ± 3.936) vs. (30.130 ± 4.188) , P = 0.003]. The number of neovascularization was less [(80.267 ± 13.094) vs. (162.637 ± 73.112), P = 0.022]. Conclusion: Pioglitazone can improve the stability of plaque and reduce the rupture rate of vulnerable plaque by reducing the degree of plaque inflammation.