摘要
目的探讨小鼠心肌梗死后血清细胞因子表达的变化与心肌炎症反应的关系。方法冠状动脉结扎法复制小鼠心肌梗死模型,采用ELISA方法测定结扎后不同时间点血清肿瘤坏死因子α、白细胞介素6和白细胞介素10浓度和心肌组织病理变化。结果心肌梗死后1h,小鼠血清中肿瘤坏死因子α和白细胞介素10浓度分别是82.4±27.6ng/L和47.7±22.3ng/L,与假手术组水平(40.4±9.7ng/L和23.4±4.3ng/L)比较均明显提高,差异有统计学意义(P<0.05),以后呈逐渐下降趋势;血清中白细胞介素6水平在心肌梗死后1h、2h、4h、1d、2d和5d分别为202.7±89.5ng/L、578.9±198.0ng/L、696.8±104.7ng/L、325.1±131.7ng/L、218.5±16.0ng/L和195.8±93.1ng/L,与假手术组水平(54.0±3.0ng/L)比较均有显著增高(P<0.05),病理切片显示梗死心肌内大量的炎性细胞浸润。梗死后第2至4周细胞因子表达下降,梗死区炎症细胞逐渐减少,心肌纤维化。结论肿瘤坏死因子α、白细胞介素6和白细胞介素10三种细胞因子参与了心肌梗死后心肌的炎症反应,在心肌梗死的发生发展过程中起重要作用。
Aim To investigate the relationship between cytokines expression and inflammatory response after myocardial infarction in mice. Methods Develope mice model of myocardial infarction by coronary artery ligation. Levels of serum tumor necrosis factor-α, interleukin- 6 and intedeukin- 10 were assayed by ELISA, and pathology of myocardium was detected by histochemistry. Results Expressions of tumor neerosis factor-α （82.4±27.6 ng/L） and interleukin- 10 （47.7±22.3 ng/L） were found to be significantly higher in 1 h after myocardial infarction than that of sham operated groups （40.4 ± 9.7 ng/L and 23.4±4.3 ng/L）, and they decreased gradually after that; Expressions of intedeukin- 6 （202.7 ± 89.5 ng/L, 578.9 ± 198.0 ng/L, 696.8 ± 104.7 ng/L, 325.1 ± 131.7 ng/L, 218.5 ± 16.0 ng/L, and 195.8 ± 93.1 ng/L） were also found to be significandy higher in 1 h, 2 h, 4 h, 1 d, 2 d, and 5 d after myocardial infarction than that of sham operated groups （54.0 ± 3.0 ng/ L）. Leucocytes recruited in the infarcted myocardium after myocardial infarction. Inflammatory cytokines decreased during 2 weeks and 4 weeks after myocardial infarction, and Leucocytes in the infarcted myocardium decreased gradually. Myocardium fibrosis was found. Conclusion The changes of tumor necrosis factor-α, intedeukin-6 and interleukin-10 take part in the inflammatory response after myocardial infarction, and play an important role in the development of myocardial infarction diseases.
出处
《中国动脉硬化杂志》
CAS
CSCD
2007年第4期245-247,共3页
Chinese Journal of Arteriosclerosis
基金
国家973计划项目(2001CB509904)资助
