P8 Hydrogen sulfide and SPRC mitigate infarct of myocardial infarction via governing migration and infilitration of macrophages

Background Myocardial infarction (MI), associated with the inflammatory response, has long been postulated to be key determinant of rapid necrosis of cardiac myocytes. As a part of the robust inflammatory response, activated macrophages infiltrating into the necrotic myocardium is prerequisite for healing process and scar formation during the post-infarction remodeling. Hydrogen sulfide (H 2 S) and S-propargyl-l-cysteine (SPRC) have been shown to have potent cyto-protective effects. Thus, the present study was to evaluate the roles and mechanisms of NaHS and SPRC on macrophage during infarct repair. Results Echocardiographic analysis showed that ejection fraction (EF) and fractional shortening (FS) were improved in mice pretreated with NaHS and SPRC (67 ± 6%, 77 ± 8%) compared to saline (47 ± 6%) at day 5 post-MI. Concomitantly, 3, 5 and 8 days after MI, the cardiac tissues of NaHS and SPRC groups exerted an increase in immunohistochemical staining for macrophage markers (Galectin-3). And the mRNA levels of Galectin-3 and F4/80 were also increased significantly. In addition, both SPRC and NaHS trigged decreased levels of IL-1beta, IL-6, and TNF- α , which were mainly produced by M1 macrophages, but increased levels of IL-10 and CD163, which were partially due to the activation of reparative M2 Macrophages. In addition, transwell assay revealed that NaHS and SPRC accelerated the migration of peritoneal macrophages, and the immunofluorescence analysis indicated a promoted reorganization of actin cytoskeleton. Conclusion NaHS and SPRC may have potential as an anti-infarct of MI, through governing migration and infilitration of macrophages.