Objective To observe the effect of electroacupuncture(EA)at “Baihui”(GV20) and “Shenting”(GV24) on the expression of melatonin synthesis rate-limiting enzyme―arylalkylamine N-acetyltransferase(AANAT)in pineal gland of rats with focal cerebral ischemia-reperfusion injury

so as to explore the mechanism of EA underlying improving ischemia-reperfusion injury.Methods Forty-eight SD rats were randomly divided into sham operation

model

EA and non-acupoint groups

with 12 rats in each group. The focal cerebral ischemia-reperfusion injury rat model was established by occlusion of the middle cerebral artery. Rats of the EA group received EA at GV20 and GV24

while those in the non-acupoint group received EA at non-acupoints below the costal margins on both sides for 20 min

once daily for 7 days. The neurological deficit score(0 to 4 points) was given after successful modeling according to Longa's method. Morris water maze test was used to assess the cognitive function of rat. ELISA was used to detect the plasma melatonin content

and PCR and Western blot were used to detect the mRNA and protein expressions of AANAT in the pineal gland

separately. Immunofluorescence staining was used to detect the activation of astrocytes and neuronal injury in the hippocampus.Results After focal cerebral ischemia-reperfusion injury and compared with the sham operation group

the neurological deficit score

the escape latency

and the expression of GFAP were significantly increased(P<0.01)

while the times of platform quadrant crossing

the secretion of melatonin at 24:00

AANAT mRNA and protein expression levels and NeuN protein expression were significantly down-regulated(P<0.01). After EA at GV20 and GV24

the above-mentioned indexes all reversed in the EA group relative to the model group

and there were significant differences between the two groups(P<0.01). Compared with the model group

the changes of the abovementioned indexes in the non-acupoint group were not statistically significant(P>0.05).Conclusion EA at GV20 and GV24 can alleviate neurological deficit and improve cognitive function in cerebral ischemia-reperfusion rats

which may be related to its effects in up-regulating endogenous melatonin levels

inhibiting the activation of astrocytes and protecting damaged neurons in the hippocampus.