论文部分内容阅读
AIM:To study the effects of tetrandrine(Tet)on calciumrelease-activated calcium current(I_(CRAC)),delayed rectifierpotassium current(I_K),and inward rectifier potassiumcurrents(/_(K1))in isolated rat hepatocytes.METHODS:Hepatocytes of rat were isolated by usingperfusion method.Whole cell patch-clamp techniques wereused in our experiment.RESULTS:The peak amplitude of I_(CRAC)was-508±115 pA(n=15),its reversal potential of I_(CRAC)was about 0 mV.At thepotential of -100 mV,Tet inhibited the peak amplitude ofI_(CRAC)from -521±95 pA to -338±85 pA(P<0.01 vs control,n=5),with the inhibitory rate of 35 % at 10μmol/L andfrom -504±87 pA to -247±82 pA(P<0.01 vs control,n=5),with the inhibitory rate of 49% at 100μmol/L,withoutaffecting its reversal potential.The amplitude of I_(CRAC)wasdependent on extracellular Ca~(2+)concentration.The peakamplitude of I_(CRAC)was -205±105 pA(n=3)in tyrode’s solutionwith Ca~(2+)1.8 mmol/L(P<0.01 vs the peak amplitude ofI_(CRAC)in external solution with Ca~(2+)10 mmol/L).Tet at theconcentration of 10 and 100μmol/L did not markedly changethe peak amplitude of delayed rectifier potassium currentand inward rectifier potassium current(P>0.05 vs control).CONCLUSION:Tet protects hepatocytes by inhibiting I_(CRAC),which is not related to I_K and I_(K1).
AIM: To study the effects of tetrandrine (Tet) on calciumrelease-activated calcium current (I_ (CRAC)), delayed rectifierpotassium current (I_K), and inward rectifier potassiumcurrents (/ _ (K1)) in isolated rat hepatocytes. METHODS: Hepatocytes of rat were isolated by using perfusion method. Whole cell patch-clamp techniques were used in our experiment .RESULTS: The peak amplitude of I_ (CRAC) was-508 ± 115 pA (n = 15) about 0 mV.At the potential of -100 mV, Tet inhibited the peak amplitude of I_ (CRAC) from -521 ± 95 pA to -338 ± 85 pA (P <0.01 vs control, n = 5) with the inhibitory rate of 35 % at 10 μmol / L and from -504 ± 87 pA to -247 ± 82 pA (P <0.01 versus control, n = 5) with the inhibitory rate of 49% at 100 μmol / L, without effect on its reversal potential. (CRAC) was -205 ± 105 pA (n = 3) in tyrode’s solution with Ca 2+ 1.8 mmol / L (P <0.01 vs the peak amplitude of I_ (CRAC) in external solution with Ca ~ (2+) 10 mmol / L) .Tet at the concentration of 10 and 100 μmol / L did not markedly change the peak amplitude of delayed rectifier potassium current and inwardly rectified potassium current (P> 0.05 vs control) .CONCLUSION: Tet protects hepatocytes by inhibiting I_ (CRAC), which is not related to I_K and I_ (K1).