摘要
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(tumornecrosis factoralpha,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(23722±8671)pgvs(17693±5705)pg,P<0.05;IL-1β(335±95)pgvs(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。
Objective : To compare the different expressions of cardiac inflammatory cytokines including tumor necrosis factor-alpha ( TNF-α), interleukin-1β ( IL-1β), 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-1 [3 both increased significantly in CA groups [ IL-6 ( 23 722 ±8 671 ) pg vs ( 17 693 ±5 705 ) pg, P 〈 0.05 ; IL-1 β (335 ± 95 ) pg vs ( 159 ± 99) pg, P 〈 0.01 ]. There was no difference of TNF-α between operated and sham-operated groups in ACF or CA groups . Conclusion : The contents of IL-6 and IL-1 β in myocardium increased in pressure overload-induced cardiac hypertrophy.
出处
《北京大学学报(医学版)》
CAS
CSCD
北大核心
2007年第6期570-575,共6页
Journal of Peking University:Health Sciences
基金
国家自然科学基金(30470691)
国家重点基础研究发展规划项目基金(2006CB503806)资助~~