不同类型心脏肥大大鼠模型心肌中炎症细胞因子表达差异

目的:比较压力负荷型和容量负荷型心脏肥大大鼠模型心肌中炎症细胞因子的表达差异. 方法:采用腹主动脉-下腔静脉造瘘法复制容量负荷型心脏肥大大鼠模型,主动脉缩窄法复制压力负荷型心脏肥大大鼠模型.分别在术后1周和2周对模型进行心脏称重、组织切片检查,并检测左心室心肌中炎症细胞因子肿瘤坏死因子α(tumor necrosis factor alpha ,TNF-α)、白细胞介素6(interleukin-6,IL-6)和白细胞介素1β(interleukin-1β,IL-1β)的含量.结果: 两种模型的手术组于1周和2周时均出现心脏肥大,压力负荷手术组心肌组织切片可见明显胶原增生.左心室IL-6和 IL-1β总含量在压力负荷手术组明显大于假手术组IL-6(23 722±8 671)pg vs (17 693±5 705)pg,P《0.05;IL-1β(335±95)pg vs (159±99)pg,P《0.01].左心室TNF-α总含量在压力负荷和容量负荷组,手术组与假手术组相比较差异均无统计学意义(P》0.05).结论: 在心脏肥大的病理进程中,心肌组织中炎症细胞因子IL-6和IL-1β的含量发生了变化;在压力负荷所致心脏肥大的心肌中IL-6和IL-1β含量明显增加.

Different expressions of inflammatory cytokines in two types of cardiac hypertrophy in rats

OBJECTIVE: To compare the different expressions of cardiac inflammatory cytokines including tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta(IL-1beta), interleukin-6 (IL-6) in two types of cardiac hypertrophy rat models induced by volume overload and pressure overload. METHODS: Volume overload-induced cardiac hypertrophy was established by abdominal aortacaval fistula (ACF) and pressure overload-induced cardiac hypertrophy was developed by constriction of aorta (CA). Heart weight measurement and histological examination were performed 1 week or 2 weeks after the operation respectively. The cytokine expression was measured by enzyme linked immunosorbent assay. RESULTS: All the operated groups developed cardiac hypertrophy. The left ventricular fractional shortening of each operated group had no significant difference with the sham-operated groups respectively. As far as the total amount of each cytokine in left ventricular myocardium was concerned, compared to the sham-operated groups, IL-6 and IL-1beta both increased significantly in CA groups IL-6(23 722+/-8 671)pg vs (17 693+/-5 705)pg,P<0.05 ;IL-1beta(335+/-95)pg vs (159+/-99) pg,P<0.01].There was no difference of TNF-alpha between operated and sham-operated groups in ACF or CA groups . CONCLUSION: The contents of IL-6 and IL-1beta in myocardium increased in pressure overload-induced cardiac hypertrophy.