Objective To investigate the effect of electroacupuncture(EA) on intestinal Toll-like receptor 4(TLR4) and nuclear factor-kappa B(NF-κB) in obese rats

so as to explore the mechanism of action of acupuncture in losing weight. Me-thods A total of 50 male Wistar rats were randomly divided into control and model groups. High-fat feed was used to establish a rat model of obesity

and after modeling

the 24 rats were randomly divided into model group

TLR4 inhibitor group

and EA group

with 8 rats in each group. The rats in the EA group were given EA at "Guanyuan"(CV4)

"Zhongwan "(CV12)

"Zusanli"(ST36)

and" Fenglong"(ST40)

10 minutes each time

3 times a week

and those in the TLR4 inhibitor group were given intraperitoneal injection of TAK-242 three times a week; the course of treatment was 8 weeks for both groups. Body weight and blood glucose were measured every two weeks. Co-immunoprecipitation was used to observe the interaction between TLR4 and NF-κB p65 in the intestinal tissue; electrophoretic mobility shift assay was used to measure the activity of NF-κB p65; Western blot was used to measure the protein expression of TLR4

phosphorylated nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor alpha(p-IκBα)

and NF-κB p65; quantitative real-time PCR was used to measure the mRNA expression of TLR4

NF-κB p65

and IκBα. Results Compared with the control group

the model group had significant increases in body weight

blood glucose

and protein and mRNA expression of TLR4 and NF-κB p65(P<0.01

P<0.05)

as well as significant enhancement in the interaction between TLR4 and NF-κB p65 and activity of NF-κB p65(P<0.05

P<0.01). Compared with the model group

the EA group had a significant reduction in body weight(P<0.05)

both of the EA group and the TLR4 inhibitor group had significant reductions in blood glucose

and protein and mRNA expression of TLR4

p-IκBα

and NF-κB p65(P<0.05

P<0.01)

as well as significant reductions in the activity of NF-κB p65(P<0.01). Conclusion EA can effectively regulate intestinal TLR4

inhibit the interaction between TLR4 and NF-κB p65

and reduce the activity of NF-κB p65

which may be a potential mechanism of EA in reducing body weight and blood glucose in obese rats.