Objective To observe the effect of electroacupuncture(EA)on neurological behavior and activity of Tolllike receptor 2/nuclear factor kappa B(TLR2/NF-κB)signaling of the ischemic cerebral area in cerebral ischemia-reperfusion injury(CIRI)rats

so as to explore its mechanisms underlying improvement of CIRI.Methods A total of 120 male SD rats were randomly divided into blank control

sham operation

model

EA and EA+NF-κB inhibitor(Pyrrolidine Dithiocarbamate Hydrochloride

PDTC

EA+PDTC)groups which were further divided into 3

7

14 and 28 dsubgroups(n=6 in each subgroup).The CIRI model was established by occlusion of the middle cerebral artery for 90 min

followed by reperfusion.EA(1-20 Hz

6 V)was applied to"Shuigou"(GV26)

"Neiguan"(PC6)

"Sanyinjiao"(SP6)and"Weizhong"(BL40)for 30 min

once a day for 28 days.For rats of the EA+PDTC group

PDTC solution(120 mg/kg)was intraperitoneally injected on the 3 rd day after successful modeling and before EA intervention.The neurological deficit severity(Zea Longa score)was assessed 3

7

14 and 28 days after modeling.The expression levels of TLR2

Interleukin-1 receptor-associated kinase(IRAK)and NF-κB mRNAs in the ischemic penumbra region of brain tissue were detected by real-time fluorescence quantitative PCR.Results Following modeling

the neurological deficit scores were significantly increased from the 3 rd day on after CIRI(P<0.05)

the expression levels of TLR2 mRNA on day 3

7

14 and 28

and IRAK mRNA on day 3 and 7

as well as NF-κB mRNA on day 3

7 and 14 were significantly up-regulated in the model group relevant to the blank control group(P<0.05).After EA intervention

the neurological deficit scores were significantly decreased in the EA group on day 3

7 and 28 and in the EA+PDTC group on day 3

7

14 and 28 in comparison with those of the model group(P<0.05).In addition

the expression levels of TLR2 mRNA and NF-κB mRNA on day3

7 and 14 in the EA group

and on day 3

7

14 and 28 in the EA+PDTC group

IRAK mRNA on day 3 in the EA and EA+PDTC group were significantly down-regulated(P<0.05)

but those of IRAK mRNA on day 14 and 28 in the EA group were significantly up-regulated in comparison with those of the model group(P<0.05).The effect of the EA+PDTC was obviously superior to that of simple EA in down-regulating the expression of TLR2(on day 28)

and IRAK(on day 3

14

28)

and NF-κB(on day 3

7 and14)(all P<0.05).Conclusion EA stimulation can improve the symptoms of neurological deficits in CIRI rats

which may be related to its effect in suppressing the expression of TLR2

NF-κB and IRAK mRNAs of the ischemic cerebral tissue

i.e.

down-regulating the activity of TLR2/NF-κB signaling.