Objective To evaluate the effect of electroacupuncture(EA) of the auricular concha(EA-AC) on serum cytokines contents and pulmonary transcription factor nuclear factor-κB(NF-κB) expression in lipopolysaccharide(LPS) induced endotoxaemia rats so as to study its mechanism underlying cholinergic anti-inflammatory efficacy.Methods Male SD rats were randomized into normal control

model(LPS)

simple EA-AC

EA-AC+LPS

vagal nerve stimulation(VNS)+LPS

and EA-Zusanli(ST 36)+LPS groups(n=12/group).Endotoxaemia model was duplicated by intravenous(tail vein) injection of LPS(0.5 mL/kg).Two intradermal needles were inserted into the central sites of the cavity of concha and cymba of auricular concha respectively on each side and stimulated electrically by using an electrical stimulator(i.e.

EA-AC).VNS was applied to the left cervical vagal nerve

and EA(1 mA

10 Hz

pulse-width 1 ms) was also applied to bilateral "Zusanli"(ST 36).Serum cytokines(TNF-α

IL-6) contents 2 h after modeling were determined by using enzyme linked immunosorbent assay(ELISA)

and pulmonary NF-κB p 65 expression 2 h after modeling was detected by using western blotting.Results Compared with the normal control group

serum TNF-α and IL-6 contents

and pulmonary NF-κB p 65 expression level in the model group were increased significantly(P<0.01).In comparison with the model group

serum TNF-α contents in the simple EA-AC

EA-AC+LPS

VNS+LPS and ST 36+LPS groups

and serum IL-6 contents and pulmonary NF-κB p 65 expression levels in the simple EA-AC

EA-AC+LPS and VNS+LPS groups were down-regulated considerably(P<0.05

P<0.01).Compared with the VNS+LPS group

serum TNF-α and IL-6 contents

and pulmonary NF-κB p 65 expression level in the ST 36+LPS group were increased significantly(P<0.05

P<0.01).In comparison with the EA-AC+LPS group

pulmonary NF-κB p 65 expression level in the ST 36+LPS group was increased remarkably(P<0.05).Conclusion Both EA of auricular concha and vagus nerve stimulation can significantly lower serum TNF-α and IL-6 contents

and down-regulate pulmonary NF-κB p 65 expression level in endotoxaemia rats

suggesting a similar cholinergic anti-inflammatory mechanism between them.