Article Text

Electroacupuncture exerts an anti-inflammatory effect in a rat tissue chamber model of inflammation via suppression of NF-κB activation
  1. Fang Liu1,2,
  2. Jianqiao Fang1,
  3. Xiaomei Shao1,
  4. Yi Liang1,
  5. Yuanyuan Wu1,
  6. Yabei Jin2
  1. 1Department of Neurobiology and Acupuncture Research, The Third Clinical Medical College, Zhejiang Chinese Medical University, Hangzhou, Zhejiang Provicine, China
  2. 2Department of acu-moxibusion, Zhejiang Hospital of Integrated Chinese & Western Medicine, Hangzhou, China
  1. Correspondence to Dr Jianqiao Fang, Department of Neurobiology and Acupuncture Research, The Third Clinical Medical College, Zhejiang Chinese Medical University, 548 Binwen Road, Hangzhou, Zhejiang Provicine, 310053, China; fangjianqiao7532{at}


Objective Electroacupuncture (EA) has beneficial effects in patients with various inflammatory diseases. However, the underlying mechanism remains unclear. As the kappa B inhibitor/nuclear factor-kappa B (IκB/NF-κB) pathway exerts a pivotal role in the mammalian immune response, we examined the involvement of the IκB/NF-κB pathway in EA-induced anti-inflammation.

Methods Ninety tissue chamber implanted rats were randomly divided into control (C), model (M) and EA (E) groups. Physiological saline and human recombinant interleukin-1β (hr IL-1β) were injected into the rats in groups C and M, respectively, and EA treatment was applied to the rats in group E after IL-1β injection. Nuclear staining of p65 (a subunit of NF-κB) was quantified in the exudate cells by immunohistochemical analysis and IκBα expression in the cytoplasm was quantified by western blot analysis.

Results Our results showed that, compared with group C, the percentage of cells with nuclear-localised p65 was increased in group M by 71.3%, 50.7% and 33.1% at 1, 5 and 24 h time points (p<0.01), respectively. This increase was fully inhibited in group E at 5 and 24 h time points (p<0.01). The expression of IκBα was stably enhanced in group M (p<0.05) during the test period. Compared with group M, greater expression of IκBα in group E was only observed at the 1 h time point (p<0.01).

Conclusions Collectively, our data suggest that EA inhibits the nuclear translocation of p65 and increases the expression of IκBα, which leads to the suppression of NF-κB activation in a rat tissue chamber model of inflammation.

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