Effect of Electroacupuncture Stimulation of“Neiguan”(PC 6)on Expression of Alpha-and Beta-subunit Proteins of Voltage-gated Sodium Channels in Rats with Myocardial Ischemia

BIAN Di; CHEN Yi-guo; SUI Yue-jiao; TIAN Hui; LIU Yu-li; CAO Rui; LI Cheng-lin; LI Bao-yan

doi:10.13702/j.1000-0607.2015.01.009

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Effect of Electroacupuncture Stimulation of“Neiguan”(PC 6)on Expression of Alpha-and Beta-subunit Proteins of Voltage-gated Sodium Channels in Rats with Myocardial Ischemia

更新时间：2023-08-11

- Effect of Electroacupuncture Stimulation of“Neiguan”(PC 6)on Expression of Alpha-and Beta-subunit Proteins of Voltage-gated Sodium Channels in Rats with Myocardial Ischemia
- Acupuncture Research Vol. 40, Issue 1, Pages: 45-49(2015)
- 作者机构：
  
  辽宁中医药大学针灸推拿学院
- 作者简介：
- 基金信息：
- DOI：10.13702/j.1000-0607.2015.01.009
  CLC：
- Published：2015
- 稿件说明：
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BIAN Di, CHEN Yi-guo, SUI Yue-jiao, et al. Effect of Electroacupuncture Stimulation of“Neiguan”(PC 6)on Expression of Alpha-and Beta-subunit Proteins of Voltage-gated Sodium Channels in Rats with Myocardial Ischemia[J]. Acupuncture research, 2015, 40(1): 45-49.
DOI：

BIAN Di, CHEN Yi-guo, SUI Yue-jiao, et al. Effect of Electroacupuncture Stimulation of“Neiguan”(PC 6)on Expression of Alpha-and Beta-subunit Proteins of Voltage-gated Sodium Channels in Rats with Myocardial Ischemia[J]. Acupuncture research, 2015, 40(1): 45-49. DOI： 10.13702/j.1000-0607.2015.01.009.

摘要

目的:观察电针"内关"穴对心肌电压-门控钠离子通道α亚单位Nav 1.5和β亚单位1-4(Navβ1-β4)蛋白表达的调控作用

探讨电针对缺血心肌的保护机制。方法:SD大鼠随机分成空白组、模型组、非经非穴组、内关组、列缺组

每组12只。采用皮下异丙肾上腺素注射复制心肌缺血模型。内关组和列缺组分别电针双侧"内关""列缺"

每次20min

每日1次

共治疗7d。应用Western blot法检测心肌Nav 1.5和β1、β2、β3、β4的蛋白表达水平。结果:模型组心肌Nav 1.5蛋白表达水平明显低于空白组(P<0.01)

内关组和列缺组较模型组表达水平均明显增加(P<0.01)

内关组心肌Nav 1.5蛋白表达水平较列缺组显著上调(P<0.05);模型组心肌β1、β2、β3、β4蛋白表达水平均显著低于空白组(P<0.01)

内关组和列缺组与模型组比较

心肌β1、β2、β3、β4蛋白表达水平均显著增加(P<0.01)

内关组与列缺组比较

β1、β2、β3蛋白表达水平的差异有统计学意义(P<0.05)。结论:电针"内关"可能通过上调心肌电压-门控钠离子通道α亚单位和β亚单位的蛋白表达水平实现对钙超载的调节

进而改善心肌缺血状态

为经穴效应循经特异性理论提供有力的实验基础。

Abstract

Objective To observe the effect of electroacupuncture(EA)stimulation of"Neiguan"(PC 6)on expression of sodium(Nav)channelα-subunit 1.5and Navβ-subunitsβ1—β4(the known myocardial sodium channel proteins)in acute myocardial ischemia(AMI)rats so as to explore its mechanisms underlying protection of ischemic myocardium.Methods Sixty SD male rats were randomly divided into normal control

AMI model

Neiguan(PC 6)

Lieque(LU 7)and non-acupoint groups.The AMI model was established by intravenous injection of Isoprenaline(85mg/kg)once daily for 2days.Myocardial Nav1.5and Navβ1

β2

β3

β4protein expression levels were detected by Western blot.Results In comparison with the control group

myocardial Nav 1.5

β1

β2

β3andβ4protein expression levels were significantly down-regulated in the AMI model group(P<0.01).After EA stimulation

compared with the model group

the expression levels of Nav 1.5

Navβ1

β2

β3andβ4protein expression levels were significantly up-regulated in the Neiguang(PC 6)and Lieque(LU 7)groups(P<0.01)rather than in the non-acupoint group(P>0.05).There was no statistical significance between the Neiguan(PC 6)and Lieque(LU 7)groups inβ4protein expression level(P>0.05).Conclusion EA stimulation of both PC 6and LU 7can significantly reverse AMI-induced down-regulation of myocardial Nav 1.5

β1

β2

β3andβ4protein expression levels in AMI rats

which might contribute to its function in improving AMI by reducing calcium overload.

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