Fang Liu1, Jianqiao Fang2, Xiaomei Shao2, Yi Liang2, Yuanyuan Wu2, Yabei Jin3. 1. Department of Neurobiology and Acupuncture Research, The Third Clinical Medical College, Zhejiang Chinese Medical University, Hangzhou, Zhejiang Provicine, China Department of acu-moxibusion, Zhejiang Hospital of Integrated Chinese & Western Medicine, Hangzhou, China. 2. Department of Neurobiology and Acupuncture Research, The Third Clinical Medical College, Zhejiang Chinese Medical University, Hangzhou, Zhejiang Provicine, China. 3. Department of acu-moxibusion, Zhejiang Hospital of Integrated Chinese & Western Medicine, Hangzhou, China.
Abstract
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. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.
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. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.
Authors: Suzi S Y Mansu; Haiying Liang; Shefton Parker; Meaghan E Coyle; Kaiyi Wang; Anthony L Zhang; Xinfeng Guo; Chuanjian Lu; Charlie C L Xue Journal: Evid Based Complement Alternat Med Date: 2018-03-12 Impact factor: 2.629