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AIM: To study the effects of AP-Q on CCl4-induced acute liver injury, delayed outward potassium current (Ik), inward rectifier potassium current (Ik1) and calcium release-activated calcium current (ICRAC) in isolated rat hepatocytes.METHODS: A single dose of CCl4 (10 μ g/mL, ip) was injected to induce acute liver injury in rats. Serum aminotransferase activities were determined. Whole cell patch-clamp techniques were used to investigate the effects of AP-Q on delayed outward potassium current (Ik), inward rectifier potassium current (Ik1) and calcium release-activated calcium current (ICRAC).RESULTS: AP-Q (3.5 and 7 iμg/kg) pretreatment significantly reduced ALT and AST activities. AP-Q 0.1-100 nlMl produced a concentration-dependent increase of Ik with ECs0 value of 5.55±1.8 nM (n=6). AP-Q 30 nM shifted the Ⅰ-V curve of Ik leftward and upward. CCl4 4 mM decreased Ik current 28.6±6.5% at 140 mV. After exposure to CCl4 for 5 min, AP-Q 30 nM attenuated the decrease of Ik induced by CCl4 close to normal amplitude. AP-Q 0.01-100 nM had no significant effect on either inward or outward components of Ik1 at anymembrane potential examined. AP-Q 0.1-100 nM had nosignificant influence on the peak amplitude of IcRAc, either,and did not affect the shape of its current voltage curve.CONCLUSION: AP-Q has a protective effect on CCl4-induced liver injury, probably through selectively increased Ik in hepatocytes.