CsA@PPTK significantly accumulated in ischemic myocardium, scavenged reactive oxygen species, attenuated cardiomyocyte apoptosis, reduced infarct size and fibrosis, and markedly improved heart function in a mouse model of myocardial ischemia reperfusion injury.
Does a Tregs biomimetic nanoparticle delivering Cyclosporine A (CsA@PPTK) reduce myocardial ischemia/reperfusion injury in preclinical models?
A novel platelet-membrane-coated, ROS-responsive nanoparticle delivering Cyclosporine A effectively targets ischemic myocardium and mitigates ischemia/reperfusion injury in preclinical models.
BACKGROUND: At present, patients with myocardial infarction remain an increased risk for myocardial ischemia/reperfusion injury (MI/RI). There lacks effectively method to treat MI/RI in clinic. For the treatment of MI/RI, it is still a bottleneck to effectively deliver drug to ischemic myocardium. In this paper, a regulatory T cells (Tregs) biomimetic nanoparticle (CsA@PPTK) was prepared by camouflaging nanoparticle with platelet membrane. RESULTS: CsA@PPTK actively accumulated in ischemic myocardium of MI/RI mice. CsA@PPTK significantly scavenged reactive oxygen species (ROS) and increased the generation of Tregs and the ratio of M2 type macrophage to M1 type macrophage in ischemic myocardium. Moreover, CsA@PPTK significantly attenuated apoptosis of cardiomyocytes and reduced the infarct size and fibrosis area in ischemic myocardium. CsA@PPTK markedly decreased the protein expression of MMP-9 and increased the protein expression of CX43 in ischemic myocardium tissue. Subsequently, the remodeling of the left ventricle was significant alleviated, and heart function of MI/RI mice was markedly improved. CONCLUSION: CsA@PPTK showed significant therapeutic effect on MI/RI, and it has great potential application in the treatment of MI/RI.
Li et al. (Fri,) conducted a other in Myocardial ischemia reperfusion injury (MI/RI). CsA@PPTK (Tregs biomimetic nanoparticle loaded with Cyclosporin A) vs. Normal saline, free CsA, @PPTK, CsA@PTK was evaluated on Cardiac function (LVEF, FS), infarct size, and fibrosis area. CsA@PPTK significantly accumulated in ischemic myocardium, scavenged reactive oxygen species, attenuated cardiomyocyte apoptosis, reduced infarct size and fibrosis, and markedly improved heart function in a mouse model of myocardial ischemia reperfusion injury.