Objective To explore the possible action mechanism of acupuncture at Baihui（GV20） on ischemia-reperfusion injury. Methods A total of 54 SD rats were randomized into a sham operation group

a model group and a Baihui group

with 18 rats in each group. The ischemic stroke model was established by middle cerebral artery occlusion（MCAO） surgery in the model group and the Baihui group. In the sham operation group

only the external carotid artery was ligated and no plug was inserted. Two hours after ischemia

the plug was pulled out and reperfusion was performed for 1 min and 20 h

respectively. The Baihui group was given "Baihui"（GV20） electroacupuncture stimulation

30 min each time

for 2 times. The model group and the sham operation group were only fixed for 30 min in the same way. Evans blue（EB） staining was used to detect the density of the blood-brain barrier. TTC staining was used to detect the volume of cerebral infarction. ELISA staining was used to detect the activity of histone decaproylases（HDACs）. The expression levels of HDACs subtype protein in ischemic brain tissue were detected by real-time quantitative PCR and Western blot. Results After 24 hours of ischemia-reperfusion

compared with the sham operation group

the infarct area occurred significantly in the ischemic side of the brain in the model group. EB exudation rate

HDACs activity

and the protein expression of histone decaproylase 3（HDAC3） histone decaproylase 6（HDAC6） and histone decaproylase 11（HDAC11） were increased significantly

and histone decaproylase 1（HDAC1）

histone decaproylase 2（HDAC2）

and histone decaproylase 9（HDAC9） protein expression decreased（P<0.05 or P<0.01）; after electroacupuncture intervention

compared with the model group

EB exudation rate

infarct volume

HDACs activity and HDAC3

HDAC6

and HDAC11 protein expressions decreased significantly in the Baihui group

and HDAC1

HDAC2

and HDAC9 expressions increased（P<0.05）. Conclusion Electro-acupuncture at "Baihui"（GV20） can reduce the activity of HDACs in the brain tissue of rats with ischemia-reperfusion injury

and reversely regulate the unbalanced expression of HDACs caused by ischemia-reperfusion injury

which may be one of its mechanisms of anti-brain injury.