Objective To investigate the mechanism of electroacupuncture in alleviating cerebral ischemia injury in cerebral ischemia-reperfusion rats by regulating melatonin-NOD-like receptor protein 3(NLRP3) mediated pyroptosis. Methods A total of 48 SD rats were randomly divided into sham operation group

model group

electroacupuncture(EA) group and EA +Luz group

with 12 rats in each group. The focal cerebral ischemia-reperfusion injury model was established by middle cerebral artery embolization. Rats of the EA group was treated with EA stimulation(4 Hz/20 Hz

0.5 mA

20 min) at “Baihui”(GV20) and “Shenting”(GV24) once a day for 7 consecutive days; rats of EA+Luz group were given the same EA treatment and intraperitoneally administered melatonin receptor antagonist(luzindole

30 mg/kg)

once a day for 7 consecutive days. The neurological impairment was evaluated by Zea Longa score. The level of serum melatonin content at 12:00 and 24:00 was detected by ELISA. The percentage of cerebral infarction volume was evaluated by MRI of small animals. The apoptosis rate of nerve cells in cerebral cortex of infarct side was detected by TUNEL staining. The activation of microglia cells was detected by immunofluorescence staining. The expression levels of pyroptosis-related proteins NLRP3

Caspase-1 and interleukin(IL)-1β were detected by Western blot. Results Compared with the sham operation group

the neural function score was significantly increased(P<0.01); the melatonin content was significantly decreased at 24:00(P<0.01); the percentage of cerebral infarction volume

apoptosis rate of nerve cells in cerebral cortex area of infarction side

the expressions of NLRP3

Caspase-1 and IL-1β proteins were significantly increased(P<0.01); and microglia cells were significantly activated in the model group.Compared with the model and EA +Luz groups

the nerve function score was significantly decreased(P<0.05); the percentage of cerebral infarction volume

the nerve cell apoptosis rate

the activation level of microglia cells

the expression levels of NLRP3

Caspase-1 and IL-1β were significantly decreased(P<0.01

P<0.05) in the EA group. Compared with the model and EA+Luz groups

the melatonin content at 24:00 was significantly increased(P<0.01

P<0.05) in the EA group. Conclusion EA at GV20 and GV24 can reduce the neurolo-gical injury in cerebral ischemia reperfusion model rats

which may be related to regulating the expression of endogenous melatonin

inhibiting cell scorchification and reducing cerebral ischemia injury.