New drug reduces inflammation during coronary catheterization J_Immunol
Neutrophils are critical for mediating inflammatory responses. Inhibiting neutrophil recruitment is an attractive approach for preventing inflammatory injuries, including myocardial ischemia-reperfusion injury, which exacerbates cardiomyocyte death after primary percutaneous coronary intervention in acute myocardial infarction. In this study, we found out that a neutrophil exocytosis inhibitor Nexinhib20 inhibits not only exocytosis but also neutrophil adhesion by limiting βintegrin activation.
Using a dynamic flow cytometry assay, we discovered that Nexinhib20 suppresses intracellular calcium flux and βintegrin activation after IL-8 stimulation. Western blots of Ras-related C3 botulinum toxin substrate 1 –GTP pull-down assays confirmed that Nexinhib20 inhibited Rac-1 activation in leukocytes. An in vitro competition assay showed that Nexinhib20 antagonized the binding of Rac-1 and GTP.
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