In vitro study | Gö6983 (300μm) acts on NIH3T3 cells transfected with pkcμ, inhibiting pkcμ autophosphorylation by 20%. Cardiac reperfusion PMNs and Gö 6983 (100 nM), left ventricular development pressure (LVDP) and LVDP rates recovered to 89% and 74% of baseline values, respectively, significantly higher than PMNs alone. Compared with cardiac ischemia-reperfusion (I/R)+ PMN, gö6983 (100 nM) significantly reduced PMNs adhesion to endothelial cells and infiltration into myocardium, and the release of superoxide from PMNs was significantly inhibited, up to 90%. In the presence of PMNs, Gö 6983 reduces post-I/R myocardial contractile dysfunction, which may be partially related to reduced superoxide production. The Gö 6983 significantly inhibited antigen-induced superoxide release from leukocytes of patients who had previously been allergic to tree pollen. Gö 6983 acts on human vascular tissue to inhibit intracellular Ca(2 +) accumulation, indicating the mechanism of its vasodilatory properties. Go-6983(1 μm) in combination with Ro-31-8425(390 nM) in PGSMCs slightly inhibited the activity of PLD2 induced by Angiotensin II. Gö 6983 is a subtype-specific PKC inhibitor that targets the ATP binding site. Gö 6983 inhibits Δpfpkb activity with an IC50 of 1 μm. In Gö 6983(5 μm) treated cells, the number of next cell cycle loops was significantly reduced compared to control cultures. Gö 6983 (5 μm) treatment of P. falciparum cultures reduced new ring formation by nearly 60%. |