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AIM: To study the effects of hepatic ischemia/ reperfusion (I/R) injury on store-operated calcium channel (SOC) currents (Isoc) in freshly isolated rat Kupffer cells, and the effects of Ca2+ channel blockers, 2-aminoethoxydiphenyl borate (2-APB), SK&F96365, econazole and miconazole, on Isoc in isolated rat Kupffer cells after hepatic I/R injury. METHODS: The model of rat hepatic I/R injury was established. Whole-cell patch-clamp techniques were performed to investigate the effects of 2-APB, SK&F96365, econazole and miconazole on Isoc in isolated rat Kupffer cells after hepatic I /R injury. RESULTS: I/R injury significantly increased Isoc from -80.4±25.2pA to -159.5±34.5pA (bP< 0.01, n = 30). 2-APB (20, 40, 60, 80, 100μmol/L), SK&F96365 (5, 10, 20, 40, 50μmol/L), econazole (0.1, 0.3, 1, 3, 10μmol/L) and miconazole (0.1, 0.3, 1, 3, 10μmol/L) inhibited Isoc in a concentration-dependent manner with IC50 of 37.41μmol/L (n = 8), 5.89μmol/L (n = 11), 0.21μmol/L (n = 13), and 0.28μmol/L (n = 10). The peak value of Isoc in the I-V relationship was decreased by the blockers in different concentrations, but the reverse potential of Isoc was not transformed. CONCLUSION: SOC is the main channel for the influx of Ca2+ during hepatic I/R injuries. Calcium channel .blockers, 2-APB, SK&F96365, econazole and miconazole, have obviously protective effects on I/R injury, probably by inhibiting Isoc in Kupffer cells and preventing the activation of Kupffer cells.
AIM: To study the effects of hepatic ischemia / reperfusion (I / R) injury on store-operated calcium channel (SOC) currents (Isoc) in freshly isolated rat Kupffer cells, and the effects of Ca 2+ channel blockers, 2-aminoethoxydiphenyl borate 2-APB), SK & F96365, econazole and miconazole, on Isoc in isolated rat Kupffer cells after hepatic I / R injury. METHODS: The model of rat hepatic I / R injury was established. Whole-cell patch-clamp techniques were performed to investigate the effects of 2-APB, SK & F96365, econazole and miconazole on Isoc in isolated rat Kupffer cells after hepatic I / R injury. RESULTS: I / R injury significantly increased Isoc from -80.4 ± 25.2pA to -159.5 ± 34.5pA (bP < 0.01, n = 30), 2-APB (20, 40, 60, 80, 100 μmol / L), SK & F96365 (5,10,25,05 μmol / L), econazole (0.1,3.3,1,3 and 10 μmol (N = 8), 5.89μmol / L (n = 11), 0.21μmol / L (n = μmol / L (n = 13), and 0.28 μmo l / L (n = 10). The peak value of Isoc in the IV relationship was decreased by the blockers in different concentrations, but the reverse potential of Isoc was not transformed. CONCLUSION: SOC is the main channel for the influx of Ca2 + during hepatic I / R injuries. Calcium channel. blockers, 2-APB, SK & F96365, econazole and miconazole, have obviously protective effects on I / R injury, probably by inhibiting Isoc in Kupffer cells and preventing the activation of Kupffer cells.