Objective To observe the effect of electroacupuncture(EA)preconditioning on acute myocardial ischemia(MI)and expression of Toll-like receptor 4(TLR 4)

myeloid differentiation factor 88(MyD 88)and nuclear factor-κB(NF-κB)mRNAs in the"Neiguan"(PC 6)area of rats with MI-reperfusion injury(MIRI)

so as to explore its mechanisms underlying improvement of MIRI.Methods Forty-eight male Wistar rats were randomly divided into control

control+ EA

sham operation

model

EA and sham EA groups(n=8).The MIRI model was established by occlusion of the descending anterior branch of the left coronary artery for 30 min

followed by reperfusion.Before modeling

EA preconditioning was respectively applied to PC 6 or sham PC 6 for 30 min

once daily for 5 days.Electrocardiogram(ECG)of the standard limb-leadⅡ was recorded before and after the modeling

and 0.25 hafter reperfusion.The expression levels of TLR 4

MyD 88 and NF-κB genes in the PC 6 tissue were detected by Real-time PCR.Results Compared with the control group

the height of ECG J-point was significantly increased in the model group(P<0.01)

suggesting an acute MI

and the height of J-point was significantly lower in the EA group than in the model and sham EA groups(P<0.01).In comparison with the control group

the expression levels of TLR 4

MyD 88 and NF-κB mRNAs were markedly up-regulated in the area of PC 6 in the model group(P<0.01).Compared with the model group

the increased expression levels of TLR 4

MyD 88 and NF-κB mRNAs in the EA preconditioning group were significantly inhibited(P<0.05).No significant differences were found among the control

control+EA and sham operation groups and between the model and sham EA groups in the expression levels of TLR 4

MyD 88 and NF-κB mRNAs(P>0.05).Conclusion EA preconditioning can improve myocardial ischemia and reduce the expression of TLR 4

MyD 88 and NF-κB mRNAs in PC 6 area of MIRI rats

suggesting an involvement of the regional cutaneous TLR 4/MyD 88/NF-κB signaling suppression in the initiation-transfer-amplification of EA stimulating signal inputs for relieving MIRI.