趋化因子Fractalkine与心肌细胞缺血再灌注损伤  

Expression of a novel chemokine,Fractalkine,in Myocardial Ischemia-reperfusion Injury

作　　者：潘迪光[1] 李志梁[1] 刘映峰[1] 宋旭东[1] 傅强[1] 

机构地区：[1]南方医科大学珠江医院心脏内科

出　　处：《中华高血压杂志》2007年第9期748-751,共4页Chinese Journal of Hypertension

摘　　要：目的探讨一种新的化学趋化因子Fractalkine(FKN)与缺血再灌注关系及其信号转导途径。方法分别培养心肌细胞(MC)、心肌成纤维细胞(CFs)、人脐静脉内皮细胞(ECV304),利用缺氧(缺血液)和复氧液(再灌注液)造成3种细胞的缺氧复氧模拟缺血再灌注,观察3种细胞存活率及RT-PCR检测的FKN的mRNA表达;对人脐静脉内皮细胞给NF-κB特异性抑制剂吡咯烷二硫氨基甲酸酯(PDTC),检测的FKN的mRNA表达变化。结果1)CFs在整个缺氧复氧过程中没有FKN的表达。2)ECV304缺氧前与复氧即刻FKN无表达,缺氧复氧后0.5、1、2、3、4hFKN表达增加,分别是(0.21±0.02)、(0.43±0.02)、(0.58±0.02)、(0.40±0.02)、(0.13±0.02),于复氧后2h到达表达最高值(全部P<0.01)。3)MC缺氧复氧后0.5、1、2hFKN表达增加,分别是(0.12±0.01)、(0.34±0.05)、(0.41±0.05),于复氧后2h到达表达最高值(P均<0.01)。4)每个时间段MC的FKN表达均低于ECV304(P<0.01)。5)PDTC(3、10μmol/L)是NF-κB的抑制剂,可明显抑制ECV的FKN mRNA的表达(P<0.01)。结论FKN参与心肌缺血再灌注过程,内皮细胞是表达FKN的主要细胞;NF-κB可能参与FKN表达的信号转导通路。Objection To explore the relationship between a novel chemokine, Fractalkine（FKN）, and ischernia-reperfusion injury. Methods Myocardial cells（MCs）, cardiac fibroblast（CFs） and human umbilical vein endothelial cells （ECV304） were cultured under exposure of hypoxia/reperfusion. Cell viability was calculated and rnRNA expression of FKN was assessed by RT-PCR. Results 1）No expression of FKN was detected in CFs during the whole process of ischernia-reperfusion. 2）No expression of FKN was detected in ECV304 before and immediately after ischernia-reperfusion. However, the expression of FKN in ECV304 was increased to 0.21 ± 0.02, 0.43±0.02, 0.58±0.02, 0.40±0.02 and 0.13±0.02 in 0.5, 1, 2, 3 and 4 hours after ischernia-reperfusion, with the highest expression at 2 hours after reperfusion （all P〈0.01）. 3）The expression of FKN in MCs was increased to 0. 12±0.01, 0. 34±0.05 and 0.41±0.05 in 0.5, 1 and 2 hours after ischernia-reperfusion, with the highest expression at 2 hours after reperfusion（all P〈0.01）, which were lower than that in ECV304（P〈0.01） at all time points. 4）PDTC（3 and 10 μmol/L）, a inhibitor of NF-κB, significantly inhibit the expression of FKN rnRNA in ECV（P〈0.01）. Conclusion Endothelia cells produced FKN takes part in the process of ischernia and reperfusion in myocardial cells. NF-κB may be one of the signal transduction of FKN expression.

关 键 词：缺血再灌注 趋化因子 FRACTALKINE 吡咯烷二硫氨基甲酸酯 

分 类 号：R541[医药卫生—心血管疾病]