Resistance Exercise Induces Heme Oxygenase-1 Expression to Promote Macrophage Polarization and Accelerate Catheter-related Thrombolysis and Recanalization in Rats

Abstract

IntroductionCatheter-related thrombosis (CRT) is a major complication of central venous catheters. Resistance exercise to prevent CRT formation has been demonstrated, but there are few studies of CRT dissolution and recanalization. In this study, we focused on resistance exercise, heme oxygenase-1 (HO-1), and macrophage polarization to investigate the mechanism of resistance exercise accelerating thrombolysis and recanalization, providing a theoretical basis for resistance exercise adjuvant therapy of CRT.MethodsA rat CRT model was established and Intervened with resistance exercise and injection of HO-1 agonist cobalt protoporphyrin (COPP) and the inhibitor tin protoporphyrin IX(SnPP).Thrombolysis and recanalization were observed by hematoxylin and eosin(H&E). Neovascularization was detected by immunohistochemical CD31 staining. The levels of HO-1, IL-6, and IL-10 in the rat sera were determined by enzyme-linked immunosorbent assay (ELISA). The relative expression levels of HO-1, Arg-1, HO-1, CD206, and CD80 mRNA were detected by quantitative polymerase chain reaction (qPCR). The colocalization expression of HO-1 with CD206 and CD86 were detected by immunofluorescence.ResultsResistance exercise for 28 days could induce HO-1 expression, decrease IL-6 level, increase IL-10 level, increase Arg-1 and CD206 expression, decrease INOS and CD80 expression, and increase CD31 expression, and the co-localization expression of HO-1 and CD206 was significantly higher than that of HO-1 and CD86.ConclusionAfter 28 days of resistance exercise, mechanical stimulation can mediate the expression of HO-1 in macrophages, promote the polarization of M2 macrophages, exert the effects of anti-inflammation and promoting angiogenesis, and accelerate the dissolution and recanalization of CRT.