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目的研究芍药苷对小鼠急性心肌梗死(AMI)心室重构的作用及其相关机制。方法实验采用手术构建AMI小鼠模型,根据饮食不同分为对照组,模型组,低剂量芍药苷组,高剂量芍药苷组。记录2周内心脏破裂发生率,超声探查心脏改变,逆转录(Real-time)PCR分析心室中炎症基因白细胞介素-6、转化生长因子-α、血管细胞黏附因子-1、核因子-κB(IL-6、TFN-α、VCAM-1、NF-κB)、重构相关基因(MMP-2,9,TIMP-2)的表达。结果模型组心脏破裂率为43.8%,而低高两个剂量组心脏破裂率均为12.5%。心脏超声提示芍药苷干预后心脏扩大程度减弱、心室壁稍变薄、收缩力增强,整体心室重构程度较轻(P<0.05),但不同剂量组间未见差异性(P>0.05)。Real-Time PCR结果显示,模型组小鼠心室炎症基因及重构相关基因基质金属蛋白(MMP-2,MMP-9)表达均显著上调(P<0.05),且TIMP-2表达降低,芍药苷干预后明显逆转(P<0.05),且与剂量有关。结论芍药苷能够降低心脏破裂率,改善心室结构,减轻心脏重构,这一作用可能与调控NF-κB减少局部炎症及抑制基质金属蛋白酶活力有密切关系。
Objective To study the effect and mechanism of paeoniflorin on ventricular remodeling in mice with acute myocardial infarction (AMI). Methods The AMI mouse model was constructed by surgery. According to the diet, the rats were divided into control group, model group, low dose paeoniflorin group and high dose paeoniflorin group. The incidence of heart rupture was recorded within 2 weeks. The cardiac changes were detected by ultrasound. Real-time PCR analysis of ventricular inflammatory cytokines interleukin-6, transforming growth factor-α, vascular cell adhesion molecule-1, nuclear factor- (IL-6, TFN-α, VCAM-1, NF-κB) and remodeling related genes (MMP-2,9 and TIMP-2) Results The rate of heart rupture in model group was 43.8%, while the rate of heart rupture in model group was 12.5%. Cardiac echocardiography showed that the degree of heart enlargement was weakened after paeoniflorin intervention, the ventricular wall thinned slightly, the contractility was enhanced, and the degree of global ventricular remodeling was lighter (P <0.05), but no difference was found between different dose groups (P> 0.05). Real-Time PCR results showed that the expressions of MMP-2 and MMP-9 in model group were significantly increased (P <0.05), and the expression of TIMP-2 was decreased. The expression of paeoniflorin After the intervention significantly reversed (P <0.05), and dose-related. Conclusion Paeoniflorin can reduce the rate of heart rupture, improve ventricular structure and reduce cardiac remodeling, which may be related to the regulation of NF-κB to reduce local inflammation and inhibit matrix metalloproteinase activity.