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目的:研究苄基四氢帕马汀(BTHP)经蛋白激酶C对豚鼠心肌细胞延迟整流钾电流的作用极其在临床中的应用前景。方法:应用膜片钳在全细胞模式下记录延迟整流钾电流(Ik)。结果:PMA10.0μmol/L在细胞内给药可使Ik和Ik,tail增加,电流密度分别从(13.1±1.4)pA/pF和(5.1±0.7)pA/pF增至(19.5±0.7)pA/pF和(7.3±0.4)pA/pF。应用BTHP后上述增加效应被明显减少,BTHP的抑制作用在单独应用时为(38±6)%和(36±6)%,而在预先应用PMA后BTHP的抑制作用增加至(64±7)%和(64±6)%。结论:BTHP对Ik和Ik,tail的阻滞作用可能部分与抑制细胞内蛋白激酶C途径有关。
Objective: To investigate the effect of benzyltetrahydropalmatine (BTHP) on delayed rectifier potassium current in guinea pig cardiomyocytes via protein kinase C, which has great clinical application prospects. METHODS: Delayed rectifier potassium currents (Ik) were recorded in whole-cell mode using patch-clamp. Results: PMA10.0μmol / L increased Ik and Ik, tail and increased current density from (13.1 ± 1.4) pA / pF and (5.1 ± 0.7) pA / pF to (19.5 ± 0.7) pA / pF and (7.3 ± 0.4) pA / pF. The effect of BTHP was significantly reduced after BTHP administration. The inhibitory effect of BTHP was (38 ± 6)% and (36 ± 6)% when applied alone, while the inhibitory effect of BTHP increased to (64 ± 7) after pretreatment with PMA. % And (64 ± 6)%. Conclusion: The blocking effect of BTHP on Ik, Ik and tail may be partly related to the inhibition of intracellular protein kinase C pathway.