The programmed cell death 4/nuclear factor-κB/tumor necrosis factor α (PDCD4/NF-κB/TNF-α) signaling pathway has an important role in coronary microembolization (CME)-induced inflammation. microRNA-21 protects myocardium mainly via regulation of its target gene PDCD4. Therefore, in this study we investigated the effect of ultrasound-guided microbubble-mediated microRNA-21 transfection on cardiac function in CME pig model and determined the potential mechanisms involved. The pig CME model was established by microcatheter-mediated injection of microembolization beads into the left anterior descending artery. The CME with microRNA transfection group was injected with plasmid-microbubble mixture through the marginal ear vein 4 days before CME treatment, along with ultrasound to the myocardium. Cardiac function indices were examined by cardiac ultrasound; infarct area was measured by hematoxylin-eosin and hematoxylin-basic Fuchsin-picric acid staining of tissue pathological sections; green fluorescent protein-labeled gene expression levels were evaluated by fluorescent microscopy in frozen sections; myocardial PDCD4 and TNF-α mRNA levels were measured by fluorescent quantitative PCR and protein levels were measured by western blotting; and NF-κB activity was tested by electrophoretic mobility shift assay. Compared with the CME group, the CME with ultrasound-mediated microRNA transfection group demonstrated improved CME-induced cardiac dysfunction (P<0.05). Compared with the CME group, the CME with ultrasound-mediated microRNA transfection group showed significantly lower PDCD4 expression and NF-κB activity (P<0.05). Ultrasound microbubble-mediated microRNA-21 transfection effectively improved CME-induced cardiac dysfunction via inhibition of PDCD4/NF-κB/TNF-α signal transduction pathway.

Blood cardioplegia in cardiac surgery contains leukocytes, which causes the inflammatory reaction and promotes myocardial reperfusion injury. The removal of leukocytes from the cardioplegia line, using specialized filters, has been proposed as one of the effective methods in attenuating the inflammatory response. We performed a two-level search to identify randomized, controlled trials concerning the effects of leukocyte-depleted blood cardioplegia on myocardial reperfusion injury. Sixteen studies, comprising 738 patients, met the selection criteria. There are significant reductions in creatinine kinase isoenzyme MB (CK-MB) during 4-8h postoperatively (SMD - 0.577; 95% CI -0.795 to -0.358; p=0.000), CK-MB peak (SMD - 0.713; 95% CI -1.027 to -0.400; p=0.000), troponin in the period of 4-8h postoperatively (SMD - 0.502; 95% CI -0.935 to -0.069; p=0.023), troponin peak (SMD - 0.826; 95% CI -1.373 to -0.279; p=0.003) and inotropic support (RR, 0.500; 95% CI 0.269 to 0.931; p=0.029). Leukocyte-depleted blood cardioplegia may reduce myocardial reperfusion injury in the early postoperative period, but there has been no evidence to support the clinically significant difference. Larger and more precise randomized control trials are needed to further elucidate the cardioprotective effects of cardioplegia leukofiltration.