摘要
目的探讨炎症因子IL-1β对人冠脉平滑肌细胞表达平滑肌细胞基质金属蛋白酶-3(MMP-3)和基质金属蛋白酶组织抑制剂-1(TIMP-1)的影响。方法①应用20μg/L浓度的IL-1β刺激人冠脉平滑肌细胞,分别在共同培养0、2、4、8、24、36 h后收集细胞;②应用不同浓度的IL-1β(0、5、20、40μg/L)刺激人冠脉平滑肌细胞,共同培养6 h后收集细胞;③应用实时荧光定量PCR的方法检测细胞内MMP-3和TIMP-1基因的表达量。结果同剂量IL-1β刺激下,MMP-3的表达量在2 h时就开始发生上调,8 h达高峰,而后开始下降;在不同剂量IL-1β刺激下,MMP-3的表达量在实验剂量范围内随着IL-1β的剂量加大呈上升趋势。而TIMP-1表达量在2 h时就开始发生下调,8 h达最低,而后开始上升;在不同剂量IL-1β刺激下,TIMP-1的表达量在实验剂量范围内随着IL-1β的剂量加大呈下降趋势。结论炎症因子IL-1β能促进冠脉平滑肌细胞中斑块稳定相关标记物MMP-3、TIMP-1的表达,可能是炎症在急性冠脉综合征的发生发展中起重要作用的机制之一。
Objective To elevate the effect of IL-1β on the expressions of MMP-3 and TIMP-1 genes in human coronary artery smooth muscle cells. Methods Human coronary artery smooth muscle cells were stimulated with IL-1β （20 μg/L）, RNA were isolate and culture media were collected after 0,2,4,8,24 and 36 h. Then human coronary artery smooth muscle cells were stimulated with IL-1β（0,5,20,40 μg/ L） respectively, Isolate RNA and collect culture media after 6 h. Real-time PCR was performed on RNA to detect MMP-3 ,TIMP-1 gene expressions. Results （1）In the groups of same dose, MMP-3 gene expressions were up-regulated at 2 h, and at 8 h the expressions got to peak, then began to descent;in groups of different dose of IL-1β, MMP-3 gene expressions were up-regula dose, TIMP-1 gene expressions were down-regulated at 2 h, and ted with the dose. （2）In the groups of same at 8 h the gene expressions got to lowest, then began to go up; in groups of different dose of IL-1β, TIMP-1 gene expressions were down-regulated with the dose. Conclusion It suggested that IL-1β can promote MMP-3 gene expressions and inhibit TIMP-1 gene expressions in human coronary artery smooth muscle cells, and it may be one of the mechanisms of inflammation effect in acute coronary syndrome.
出处
《哈尔滨医科大学学报》
CAS
北大核心
2008年第4期344-347,共4页
Journal of Harbin Medical University
基金
全军医药卫生"十五"计划重点课题(04LX048)
全军医药卫生"十一五"计划科技攻关课题(06G144)
