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AIM:To study the effects of AP-Q on CCl_4-induced acuteliver injury,delayed outward potassium current (I_K),inwardrectifier potassium current (I_(K1)) and calcium release-activatedcalcium current (I_(CRAC)) in isolated rat hepatocytes.METHODS:A single dose of CCl_4 (10μg/mL,ip) was injectedto induce acute liver injury in rats.Serum aminotransferaseactivities were determined.Whole cell patch-clamptechniques were used to investigate the effects of AP-Q ondelayed outward potassium current (I_K),inward rectifierpotassium current (I_(K1)) and calcium release-activated caldumcurrent (I_(CRAC)).RESULTS:AP-Q (3.5 and 7 μg/kg) pretreatment significantlyreduced ALT and AST activities.AP-Q 0.1-100 nM produceda concentration-dependent increase of I_K with EC_(50) value of5.55±1.8 nM (n=6).AP-Q 30 nM shifted the Ⅰ-Ⅴ curve ofI_K leftward and upward.CCl_4 4 mM decreased I_K current28.6±6.5% at 140 mV.After exposure to CCl_4 for 5 min,AP-Q30 nM attenuated the decrease of I_K induced by CCl_4 closeto normal amplitude.AP-Q 0.01-100 nM had no significanteffect on either inward or outward components of I_(K1) at anymembrane potential examined.AP-Q 0.1-100 nM had nosignificant 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-inducedliver injury,probably through selectively increased I_K inhepatocytes.
AIM: To study the effects of AP-Q on CCl_4-induced acuteliver injury, delayed outward potassium current (I_K), inwardrectifier potassium current (I_ (K1)) and calcium release- activatedcalcium current (I CRAC) in isolated rat hepatocytes .METHODS: A single dose of CCl_4 (10μg / mL, ip) was injectedto induce acute liver injury in rats. Serum aminotransferaseactivities were determined.Whole cell patch-clamptechniques were used to investigate the effects of AP-Q ondelayed outward potassium current (I_K RESULTS: AP-Q (3.5 and 7 μg / kg) pretreatment significantlyreduced ALT and AST activities. AP-Q 0.1-100 (I_ (K1)) and calcium release-activated caldumcurrent nM produceda 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 ofI_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-Q30 nM attenuated the decrease of I_K induced by CCl_4 c 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 nosignificant influence on 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 -inducedliver injury, probably through selectively increased I_K inhepatocytes.