摘要
AIM: To study the effects of AP-Q on CCl4-induced acute liver injury, delayed outward potassium current (Iκ), inward rectifier potassium current (Iκ1) and calcium release-activated calcium current (ICRAC) in isolated rat hepatocytes. METHODS: A single dose of CCl4 (10 μg/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 (Iκ), inward rectifier potassium current (IKI) and calcium release-activated calcium current (ICRAC). RESULTS: AP-Q (3.5 and 7 μg/kg) pretreatment significantly reduced ALT and AST activities. AP-Q 0.1-100 nM produced a concentration-dependent increase of Iκ with EC50 value of 5.55±1.8 nM (n=6). AP-Q 30 nM shifted the I-V curve of Iκ leftward and upward. CCl4 4 mM decreased Iκ current 28.6±0.5% at 140 mV. After exposure to CCl4 for 5 rain, AP-Q 30 nM attenuated the decrease of Iκ induced by CCl4 close to normal amplitude. AP-Q 0.01-100 nM had no significant effect on either inward or outward components of Iκ1 at any membrane potential examined. AP-Q 0.1-100 nM had no significant 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 Iκ in hepatocytes.
AIM:To study the effects of AP-Q on CCl_4-induced acute liver injury,delayed outward potassium current (I_K),inward rectifier potassium current (I_(K1)) and calcium release-activated calcium current (I_(CRAC)) in isolated rat hepatocytes. METHODS:A single dose of CCl_4 (10μg/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 (I_K),inward rectifier potassium current (I_(K1)) and calcium release-activated caldum current (I_(CRAC)). RESULTS:AP-Q (3.5 and 7 μg/kg) pretreatment significantly reduced ALT and AST activities.AP-Q 0.1-100 nM produced a concentration-dependent increase of I_K with EC_(50) value of 5.55±1.8 nM (n=6).AP-Q 30 nM shifted the Ⅰ-Ⅴ curve of I_K leftward and upward.CCl_4 4 mM decreased I_K current 28.6±6.5% at 140 mV.After exposure to CCl_4 for 5 min,AP-Q 30 nM attenuated the decrease of I_K induced by CCl_4 close to normal amplitude.AP-Q 0.01-100 nM had no significant effect on either inward or outward components of I_(K1) at any membrane potential examined.AP-Q 0.1-100 nM had no significant influence on the peak amplitude of I_(CRAC),either, and did not affect the shape of its current voltage curve. CONCLUSION:AP-Q has a protective effect on CCl_4-induced liver injury,probably through selectively increased I_K in hepatocytes.
