Effects and mechanisms of store-operated calcium channel blockade on hepatic ischemia-reperfusion injury in rats

Figure 5 Store-operated calcium channel participates in hepatocellular Ca²⁺ overload in HIRI. A: I-V curves of the I_SOC induced by 10 mmol/L ethylene glycol tetraacetic acid (EGTA) in HIRI hepatocytes, recorded with voltage ramps from -100 mV to +100 mV. Red trace shows the beginning of whole-cell patch-clamp recording, the green trace shows the peak current (n = 12); B: The time course for development of I_SOC in HIRI hepatocytes (n = 12); C: I-V curves of I_SOC obtained by subtraction of baseline from peak current (the red and green sections of the trace, respectively, as described in A) at the time marked “▲” in B; D: Bar graph of the mean current density of maximal I_SOC recorded at a holding potential of -100 mV in HIRI hepatocytes (n = 12) and controls (n = 24), ^bP < 0.01; E: I_SOC was recorded in HIRI hepatocytes before (green trace) or after (black trace) the application of 100 μmol/L La³⁺ (n = 7); F: The time course of I_SOC development in the presence of 100 μmol/L La³⁺ in HIRI hepatocytes (n = 7). HIRI: Hepatic ischemia-reperfusion injury.