Background Coronary microembolization (CME) is characterized by distal microvascular occlusion. However, the inflammatory mechanisms and therapeutic targets of CME are largely unknown. Methods A total of 11 Guangxi ...Background Coronary microembolization (CME) is characterized by distal microvascular occlusion. However, the inflammatory mechanisms and therapeutic targets of CME are largely unknown. Methods A total of 11 Guangxi Bama miniature swines were divided into two groups: sham (n = 5) and CME (n = 6). Microspheres were injected into the left anterior descending artery of the CME group to make an animal model of CME. The expres- sions of microRNA-146a (miR-146a) and IRAK1, TRAF6, and AUF1 in the myocardium were detected by qPCR. Results In the CME group, microspheres, microinfarction, and inflammatory cell infiltration were found under an optical microscope. The expression levels of miR-146a were low in both groups. After CME, the expression levels of IRAK1, TRAF6, and AUF1 in the CME group were upregulated compared with those in the sham group (P 〈 0.01;P 〈 0.05;P 〈 0.05, respectively). Conclusions AUF1, IRAK1 and TRAF6, but not miR-146a, could be involved, in myocardium inflammation following CME.展开更多
基金supported by Guangxi Province Medical Technology Research and Development Project(Grant No.S201303_01)Youth Science Foundation of Guangxi Medical University(No.GXMUYSF201213)
文摘Background Coronary microembolization (CME) is characterized by distal microvascular occlusion. However, the inflammatory mechanisms and therapeutic targets of CME are largely unknown. Methods A total of 11 Guangxi Bama miniature swines were divided into two groups: sham (n = 5) and CME (n = 6). Microspheres were injected into the left anterior descending artery of the CME group to make an animal model of CME. The expres- sions of microRNA-146a (miR-146a) and IRAK1, TRAF6, and AUF1 in the myocardium were detected by qPCR. Results In the CME group, microspheres, microinfarction, and inflammatory cell infiltration were found under an optical microscope. The expression levels of miR-146a were low in both groups. After CME, the expression levels of IRAK1, TRAF6, and AUF1 in the CME group were upregulated compared with those in the sham group (P 〈 0.01;P 〈 0.05;P 〈 0.05, respectively). Conclusions AUF1, IRAK1 and TRAF6, but not miR-146a, could be involved, in myocardium inflammation following CME.