Abstract
Coronary microembolization (CME) is a common complication in percutaneous coronary intervention (PCI). Local myocardial inflammation caused by CME is the major cause of progressive cardiac dysfunction. High mobility group A1 (HMGA1)/nuclear factor-kappa B (NF-κB) signaling plays an important role in the development and progression of inflammation, but its role in CME remains unclear. This study evaluated the effect of HMGA1/NF-κB signaling on CME-induced myocardial inflammation and cardiac dysfunction. Forty Sprague-Dawley rats were randomly divided into four groups: sham, CME, CME + HMGA1 small interfering RNA (HMGA1 siRNA), and CME + scrambled siRNA (control siRNA) groups, with 10 animals each. The CME model group was established by clamping the ascending aorta and injecting microspheres through the left ventricular apex for embolization, and the sham group was established by injecting the same amount of normal saline. The HMGA1 siRNA group was injected with HMGA1 siRNA transfection complexes into the tail vein 72 h before CME modeling, and the control siRNA group was caudally injected with the same amount of scrambled siRNA 72 h before CME modeling. Twelve hours after the operation, cardiac function, serum c-troponin I level...Continue Reading
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