Objective To observe the effect of electroacupuncture(EA) preconditioning on left-cardiac function

contents of serum TNF-α and IL-6 and expression of myocardial farnesoid X receptor(FXR)

small heterodimer partner(SHP)

apoptosis inducing factor(AIF) and heat shock proteins 70(HSP70) genes in myocardial ischemia-reperfusion injury(MIRI) rats

so as to explore its mechanisms underlying improvement of ischemic myocardial injury. Methods Forty male Wistar rats were randomly divided into normal control

sham operation

MIRI model and EA pretreatment groups

with 10 rats in each group. Rats of the sham operation group received exposure of the thorax and heart. The MIRI model was established by occlusion of the anterior descending branch of the left coronary artery(LAD). EA(2 Hz/100 Hz and 1 mA) was applied to bilateral "Neiguan"(PC6)

"Zusanli"(ST36) and "Guanyuan"(CV4) for 20 min

once a day for 7 days. The left ventricular end-diastolic pressure(LVEDP)

left ventricular systolic pressure(LVSP)and maximal rates of rise and fall of left ventricular pressure(±dp/dt_(max)) were detected

the contents of serum TNF-α and IL-6 were detected by using enzyme-linked immunosorbent assay(ELISA)

and the expression of FXR

SHP

AIF and HSP70 apoptotic genes in the myocardial tissue were measured by fluorescent quantitative RT-PCR. Results Compared with the normal control group

the LVEDP

contents of serum TNF-α and IL-6

and the expression levels of myocardial FXR

SHP

AIF and HSP70 mRNAs were significantly increased(P<0.05)

while LVSP and ±dp/dt_(max) levels were obviously decreased in the model group(P<0.05). In comparison with the model group

MIRI-induced increases of LVEDP

TNF-α and IL-6 contents

and FXR

SHP and AIF mRNA expression and decreases of ±dp/dt_(max) and LVSP levels were reversed(P<0.05)

except HSP70 mRNA expression with significantly increased(P<0.05) in the EA pretreatment group. Conclusion EA pretreatment can protect the left ventricular function of the ischemic heart in MIRI rats

which may be related to its effects in reliving peripheral inflammation and regulating the expression levels of apoptosis-related factors FXR

SHP

AIF and HSP70 in the myocardium.