夹竹桃麻素对兔心房肌I<sub>K1</sub>氧化损伤的保护作用

刘岩; 刘昕; 叶加虎; 李泱; 单兆亮

doi:10.12125/j.chj.202006082

夹竹桃麻素对兔心房肌I_K1氧化损伤的保护作用

Protective effect of apocynin on oxidative damage of inward rectifier potassium current in rabbit left atrial myocytes

摘要

摘要:
目的探讨夹竹桃麻素(APO)对兔左心房肌细胞内向整流钾电流(I_K1)的保护作用。
方法运用低浓度(50 μmol/L)的过氧化氢(H₂O₂)建立氧化应激模型。应用膜片钳全细胞技术，探讨APO(100 μmol/L)对兔左心房肌细胞I_K1及动作电位时程(APD)氧化应激损伤的保护作用。Western blot检测各组兔左心房中Kir2.1蛋白的表达。反转录聚合酶联反应(RT-PCR)检测兔左心房中的KCNJ2 mRNA表达。
结果与对照组比较，低浓度H₂O₂(50 μmol/L)组I_K1峰值从(−182.2±15.6) pA/pF 下降到(−119.3±8.9)pA/pF (P<0.05)，APO(100 μmol/L)组I_K1峰值为(−175.3±15.2)pA/pF无差异；与H₂O₂组比较，H₂O₂(50 μmol/L)+APO(100 μmol/L)组I_K1峰值恢复到(−160.5±13.5)pA/pF (P<0.05)；APO使由于H₂O₂处理后减小的静息膜电位(RMP)绝对值及缩短的90%的APD(APD₉₀)得以恢复；与对照组相比，H₂O₂组Kir2.1蛋白表达下降(P<0.05)；与H₂O₂组相比，H₂O₂+APO组Kir2.1蛋白表达明显恢复(P<0.05)；与对照组相比，H₂O₂组KCNJ2 mRNA表达下降(P<0.05)；与H₂O₂组相比APO+H₂O₂组KCNJ2 mRNA表达恢复(P<0.05)
结论 APO对兔左心房肌细胞I_K1具有保护作用。

Abstract:
AIM To study the protective effect of apocynin (APO) on oxidative stress damage of inward rectifier potassium current (I_K1) in rabbit left atrial myocytes.
METHODS We made the model of oxidative stress by low level H₂O₂ (50 μmol/L). The whole cell patch clamp technique was used to study the protective effect of APO on IK1 and action potential duration (APD) under oxidative stress injury. Real-time qPCR and Western blot were used to detect the expression of KCNJ2 at mRNA and Kir2.1 protein levels.
RESULTS APO restored the peak current decreased by H₂O₂. APO also recovered the shortened resting membrane potential (RMP) and APD₉₀ caused by H₂O₂. Compared with those in H₂O₂ group, the expression of KCNJ2 mRNA and the protein levels of Kir2.1 were increased (P<0.05), which could be recovered by APO+H₂O₂.
CONCLUSION APO has some protective effect on I_K1 in left rabbit atrial myocytes.

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夹竹桃麻素对兔心房肌IK1氧化损伤的保护作用

Protective effect of apocynin on oxidative damage of inward rectifier potassium current in rabbit left atrial myocytes

夹竹桃麻素对兔心房肌I_K1氧化损伤的保护作用