Objective: To investigate the effect of electroacupuncture (EA) on brain injury in rats with cerebral ischemia-reperfusion (CI-R). Methods: A total of 104 SD rats were randomized into sham-operation (n=8)

model-Ⅰ (CI-R-24 h

n=16)

EA-Ⅰ (n=16)

medication (melatonin

3.2 mg/kg

i.p. n=8; Red Sage Injection

0.3 g/kg

i.v.

n=8)

EA+medication (n=8)

EA-prevention (n=8)

model-Ⅱ(CI-R-120 h

n=8) and EA-Ⅱ(n=8) groups. CI-R model was established by right middle cerebral artery occlusion (MCAO) for 60 min and reperfusion for 24 hours or 120 hours. EA (3 Hz

2～4 mA

continuous waves) was applied to “Dazhui” (GV 14) and “Baihui” (GV 20) for 30 min. Glutathione peroxidase (GSH-Px) and catalase (CAT) activity

and malondialdehyde (MDA) contents of the serum and hippocampus

striate body and cerebral cortex tissues were detected separately by biochemical methods. Results: Compared with sham-operation group

the activity of GSH-Px of serum and the aforementioned 3 cerebral regions of model-Ⅰ and model-Ⅱ groups decreased significantly (P<0.01)

while MDA contents of these two model groups increased considerably (P<0.01). In comparison with model-Ⅰ group

GSH-Px activity of serum and the 3 cerebral regions of EA-Ⅰ group increased significantly (P<0.05～0.01)

while MDA levels of EA-Ⅰ group lowered significantly (P<0.05). The effects of EA+red sage injection in raising GSH-Px activity and lowering MDA levels of both serum and brain tissue were markedly superior to those of EA-Ⅰ group (P<0.05～ 0.01). No significant differences were found between EA-Ⅰ and medication groups in these two indexes ( P> 0.05). Compared with model-Ⅱ group

GSH-Px activity of EA-Ⅱ in serum and the 3 cerebral regions increased significantly (P<0.05～0.01)

while their MDA contents decreased significantly ( P< 0.05～ 0.01). Conclusion: EA of GV-14 and GV-20 can prevent or inhibit CI-R-induced decrease of GSH-Px activity and increase of MDA in both blood and cerebral tissues

suggesting a good effect of EA in resisting lipid peroxidation reaction and oxygen free radical injury of CI-R

i.e.

resisting oxygen stress and protecting the brain from CI-R damage.