Objective To observe the effect of electroacupuncture(EA) on the expression of NF-κB p65 in hippocampus and the morphology of hippocampus in rats with chronic fatigue syndrome(CFS)

so as to explore its mechanism in improving cognitive dysfunction of CFS. Methods Forty-eight SD rats were randomly divided into control

model

EA and inhibitor groups(n=12 in each group). The CFS model was established by multi-factor compound stress stimulation method. Rats of the EA group received EA(50 Hz

1 mA) at “Baihui”(GV20)

Emotional Area I and bilateral Sensory Area for 30 min

once daily for 15 days. For rats in the inhibitor group

pyrrolidine dithiocarbamate(100 mg·kg

(-1)

·d(-1)·d

(-1)

) was injected intraperitoneally

once a day for 15 days. Learning and memory ability was evaluated by Morris water maze test. HE staining was used to observe the morphology of hippocampus. Western blot was used to determine the expression level of NF-κB p65 in hippocampus. Results After mode-ling

the general status score was increased(P

<

0.01)

the escape latency was prolonged(P

<

0.01)

the times of crossing the platform was decreased(P

<

0.01)

and the expression level of NF-κB p65 in hippocampus tissue was significantly increased(P

<

0.05) in the model group compared with the control group. Compared with the model group

the general status score was decreased(P

<

0.01)

the escape latency was shortened(P

<

0.01)

the times of crossing the platform was increased(P

<

0.01)

and the expression level of NF-κB p65 in hippocampus tissue was significantly decreased(P

<

0.05) in the EA and inhibitor groups. HE staining showed that in the model group

the hippocampal nerve cells were arranged disorderly

the structure was loose

and the number of apoptotic bodies and inflammatory cells was significantly increased. The degree of tissue damage of the EA and inhibitor groups was milder than that of the model group. Conclusion EA can improve the cognitive function in CFS rats

which may be associated with its effect in inhibiting the expression of NF-κB and reducing the inflammation response in hippocampus.