摘要
目的研究炎症因子白细胞介素-1β(IL-1β)、白细胞介素-6(IL-6)对人冠脉平滑肌细胞表达基质金属蛋白酶-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的IL-1β、10μg/L的IL-6刺激人冠脉平滑肌细胞,分别在共同培养0、2、4、8、24、36h后收集细胞。②应用不同浓度的IL-1β(0、5、20、40μg/L)、IL-6(0、5、10、50μg/L)刺激人冠脉平滑肌细胞,共同培养6h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TIMMP-1基因的表达量。结果同剂量IL-1β、IL-6刺激下,MMP-3的表达量在2h时就开始上调,8h达高峰,而后开始下降;在不同剂量IL-1β、IL-6刺激下,MMP-3的表达量在实验剂量范围内随着IL-1β、IL-6的剂量加大呈上升趋势(IL-1β:r=0.907,P=0.000;IL-6:r=0.919,P=0.000)。而TIMP-1表达量在2h时就开始下调,IL-1β刺激下在8h左右达最低,IL-6刺激下在4h左右达最低,而后开始上升;在不同剂量IL-1β、IL-6刺激下,TIMP-1的表达量在实验剂量范围内随着IL-1β、IL-6的剂量加大呈下降趋势(IL-1β:r=-0.768,P=0.004;IL-6:r=-0.799,P=0.002)。结论炎症因子IL-1β、IL-6对冠脉平滑肌细胞中斑块稳定相关标记物MMP-3、TIMP-1表达的影响,可能是炎症在急性冠脉综合征的发生发展中起非常重要作用的机制之一。
AIM To study the effect of interleukin-1β and interleukin-6 on matrix metalloproteinase-3 and tissue inhibitor of metalloproteinase-1 mRNA expression in human coronary artery smooth muscle cells. METHODS Human coronary artery smooth muscle cells were stimulated with interleukin-1β （20 μg/L） or interleukin-6 （ 10 μg/L）. Total RNA was isolated and culture media were collected after 0, 2, 4, 8, 24 and 36 h. Human coronary artery smooth muscle cells were stimulated respectively with interleukin-1β （0, 5, 20, 40 μg/L） or interleukin-6（0, 5, 10, 50 μg/L）. Total RNA was isolated and culture media were collected after 6h. Real-time PCR was performed on total RNA to detect mRNA expression. RESULTS With the same concentration of interleukin-1β and interleukin-6, matrix metalloproteinase-3 mRNA expression was up-regulated at 2 hours and at 8 hours the expression reached the peak and then began to descend. With different concentrations of interleukin-1β and interleukin-6, matrix metalloproteinase-3 mRNA expression was up-regulated with the increasing dose of interleukin-1β and interleukin-6 （ IL-1β ： r = 0. 907, P = 0. 000 ; IL-6 ： r = 0.919, P = 0. 000）. With the same concentration of interleukin-1β and interleukin-6, tissue inhibitor of metalloproteinase-1 mRNA expression was down-regulated at 2 hours and the mRNA expression fell to the lowest at 8 hours and 4 hours in interleukin-1β and interleukin-6 respectively, and then began to increase. With different concentrations of interleukin-1β and interleukin-6, tissue inhibitor of metalloproteinase-1 mRNA expression was down-regulated with the increasing dose of interleukin-1β and interleukin-6 （ IL-1β ： r = - 0. 768, P = 0. 004 ; IL-6 ： r = - 0. 799, P = 0. 002）. CONCLUSION Interleukin-1β and interleukin-6 promote matrix metalloproteinase-3 mRNA expression and inhibit tissue inhibitor of metalloproteinase-1 mRNA expression in human coronary artery smooth muscle cells, which may be one of the mechanisms of inflammation effect i
出处
《心脏杂志》
CAS
2008年第4期381-384,共4页
Chinese Heart Journal
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)
