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      Anti-inflammatory effects of electroacupuncture in the respiratory system of a symptomatic amyotrophic lateral sclerosis animal model.

      Neuro-Degenerative Diseases
      Adaptor Proteins, Signal Transducing, biosynthesis, Amyotrophic Lateral Sclerosis, complications, pathology, Animals, Blotting, Western, Cell Count, Cell Survival, physiology, Cytoskeletal Proteins, Electroacupuncture, Extracellular Signal-Regulated MAP Kinases, Female, Immunohistochemistry, Inflammation, therapy, Interleukin-6, Lung, metabolism, Male, Mice, Mice, Transgenic, NF-kappa B, Nuclear Proteins, Oncogene Protein v-akt, Respiratory Tract Diseases, etiology, Superoxide Dismutase, genetics, Tumor Necrosis Factor-alpha, rac GTP-Binding Proteins

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          Abstract

          Because amyotrophic lateral sclerosis (ALS) is a progressive inflammatory disease, treatment of the pulmonary system plays a key role in ALS patients' care. Previous studies have mainly examined the pathological mechanism of ALS in the central nervous system; however, there has been relatively little research regarding the pulmonary system in ALS animal models. In inflammatory diseases, including asthma and arthritis, electroacupuncture (EA) is commonly used for its anti-inflammatory effects. The goal of this study was to determine whether EA treatment affects inflammation in the pulmonary system in an ALS animal model. EA treatment at ST36 (Zusanli) acupoint was performed with 14-week-old hSOD1(G93A) transgenic mice. Immunohistochemical analysis was performed using anti-ionized calcium binding adaptor molecule 1 (Iba-1) and anti-tumor necrosis factor alpha (TNF-α) antibodies. To investigate the expression level of inflammatory proteins, Western blot analyses were performed using anti-Iba-1, anti-TNF-α, anti-nuclear factor kappa B (NF-κB), and anti-interleukin 6 (IL-6) antibodies. The activation of Ser435-phospho-specific RAC-alpha serine/threonine-protein kinase 1 (pAKT) and the increase of phosphorylated extracellular-signal-regulated kinases (pERK) protein in lung tissues of EA-treated and untreated hSOD1(G93A) mice were also evaluated by Western blot. EA treatment decreased the expression of the proinflammatory proteins such as TNF-α and IL-6, pNF-κB, and Iba-1 and increased the level of activated pAKT and pERK compared to control hSOD1(G93A) mice. Our findings suggest that EA could be an effective anti-inflammatory treatment for the respiratory impairment that occurs in ALS animal models. Copyright © 2011 S. Karger AG, Basel.

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