Objective To observe the effect of electroacupuncture(EA)stimulation of"Neiguan"(PC 6)

etc.on expression levels of myocardial chloride(CL-)channel-related genes and intracellular protein kinase C(PKC)protein in myocardial ischemia(MI)rats.Methods Seventy SD rats were randomly divided into control group(n=10)

model group(n=15)

Neiguan(PC 6)group(n=15)

Lieque(LU 7)group(n=15)and non-acupoint group(n=15).The MI model was established by i.p.of isoproterenol(ISO

a sympathomimetic beta adrenergic agonist).Electroacupuncture stimulation was applied to bilateral"Neiguan"(PC 6)

"Lieque"(LU 7)

or non-acupoint[the mid-point between"Tianshu"(ST 25)and"Shenque"(CV 8)]for 15 min

once a day for 7days.Quantitative RT-PCR was employed to detect the expression levels of cystic fibrosis transmembrane conductance regulator(CFTR

a CL-channel)mRNA and chloride channel calcium-activated 1(CLCa 1

a member of the family of calcium-activated chloride channels

CLCa)mRNA in the left cardiac ventricle tissue

and Western blot was used to detect the expression level of myocardial PKC protein of the left ventricle.Results Compared with the control group

the expression levels of myocardial PKC protein

and CLCa 1and CFTR genes were significantly increased in the model group(P<0.05).In comparison with the model group

the expression levels of myocardial PKC protein

and CFTR mRNA and CLCa 1mRNA in the Neiguan group

and PKC protein and CLCa 1mRNA in the Lieque and non-acupoint groups

as well as CFTR mRNA in the Lieque group were notably down-regulated(P<0.05).No significant change was found in the expression of CFTR mRNA in the non-acupoint group(P>0.05)

and no significant differences were found between Neiguan and Lieque groups in the expression levels of PKC protein(P>0.05).The effects of"Neiguan"(PC 6)were obviously superior to those of non-acupoint in down-regulating myocardial PKC protein

CLCa 1mRNA and CFTR mRNA(P<0.05).Conclusion EA stimulation of"Neiguan"(PC 6)can down-regulate the expression of myocardial PKC protein

CFTR and CLCa 1genes in MI rats

which may contribute to its effect in protecting myocardium from ischemic injury.