Objective To compare the effect of electroacupuncture(EA)of"Neiguan"(PC6)of the Pericardium Meridian

"Shenmen"(HT7)of the Heart Meridian

"Shuigou"(GV26)of the Governor Vessel and"Zhaohai"(KI6)of the Kidney Meridian on myocardial and cerebral cell apoptosis in cerebral ischemia(CI)rats

so as to explore its mechanism underlying improvement of CI based on the theory of"Heart-brain Correlation".Methods Forty-eight SD rats(half male and half female)were randomly divided into normal control

model

PC6

HT7

GV26 and KI6 groups(n=8 in each one).The CI model was established by occlusion of the middle cerebral artery(MCAO).EA(4 Hz/20 Hz

1.5 mA)was applied to the right PC6

HT7

GV26 or KI6 respectively for 30 min

once every 12 hfor 5 times.The cell apoptosis of the ischemic myocardial and cerebral tissues was detected by TUNEL method

and the expression of cerebral and myocardial Bax and Bcl-2 was determined by using immunohistochemistry.Results Following modeling

the cell apoptosis percentages and Bax-positive cells of both myocardial and cerebral tissues were significantly increased in the model group in comparison with the control group(P<0.01).After EA intervention

the cerebral apoptotic percentage and cerebral Bax-positive cells in the cerebral tissue of the PC6

HT7 and GV26 groups

and the myocardial apoptosis percentage in the PC6 and HT7 groups

as well as the myocardial Bax-positive cells in the PC6 group were obviously decreased(P<0.05

P<0.01)

while the cerebral Bcl-2 positive cells in the PC6

HT7 and GV26 groups

and the myocardial Bcl-2 positive cells in the PC6 and HT7 groups were significantly increased relevant to the model group(P<0.01

P<0.05).No significant changes were found in the KI 6 group in the cell apoptosis index and percentages and Baxand Bcl-2-positive cells of both myocardium and cerebral cortex tissues compared with the model group(P>0.05).Conclusion EA stimulation of PC6 and HT7 can inhibit CI injury induced cell apoptosis of cerebral and myocardial tissues in CI rats

which is possibly associated with its effects in down-regulating Bax expression and up-regulating Bcl-2 expression of both myocardial and cerebral tissues.