title: Anti-inflammatory effects of electroacupuncture in the respiratory system of a symptomatic amyotrophic lateral sclerosis animal model.
abstract: BACKGROUND
  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.
  
  
  METHODS
  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.
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  Our findings suggest that EA could be an effective anti-inflammatory treatment for the respiratory impairment that occurs in ALS animal models.
authors.affiliation: Department of Standard Research, Korea Institute of Oriental Medicine, Daejeon, Korea.
authors.forename: Jing Hua
authors.initials: JH
authors.lastname: Jiang
authors.forename: Eun Jin
authors.initials: EJ
authors.lastname: Yang
authors.forename: Myung Gi
authors.initials: MG
authors.lastname: Baek
authors.forename: Seon Hwy
authors.initials: SH
authors.lastname: Kim
authors.forename: Sang Min
authors.initials: SM
authors.lastname: Lee
authors.forename: Sun-Mi
authors.initials: SM
authors.lastname: Choi
mesh_terms: D048868:Adaptor Proteins, Signal Transducing / Q000096:biosynthesis; D000690:Amyotrophic Lateral Sclerosis / Q000150:complications* / Q000473:pathology; D000818:Animals; D015153:Blotting, Western; D002452:Cell Count; D002470:Cell Survival / Q000502:physiology; D003598:Cytoskeletal Proteins / Q000096:biosynthesis; D015671:Electroacupuncture; D048049:Extracellular Signal-Regulated MAP Kinases / Q000096:biosynthesis; D005260:Female; D007150:Immunohistochemistry; D007249:Inflammation / Q000628:therapy*; D015850:Interleukin-6 / Q000096:biosynthesis; D008168:Lung / Q000378:metabolism; D008297:Male; D051379:Mice; D008822:Mice, Transgenic; D016328:NF-kappa B / Q000096:biosynthesis; D009687:Nuclear Proteins / Q000096:biosynthesis; D051058:Oncogene Protein v-akt / Q000096:biosynthesis; D012140:Respiratory Tract Diseases / Q000209:etiology* / Q000473:pathology / Q000628:therapy*; D013482:Superoxide Dismutase / Q000235:genetics / Q000378:metabolism; D000072105:Superoxide Dismutase-1; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis; D020744:rac GTP-Binding Proteins / Q000096:biosynthesis
chemical_list: D048868:Adaptor Proteins, Signal Transducing; D003598:Cytoskeletal Proteins; D015850:Interleukin-6; D016328:NF-kappa B; D009687:Nuclear Proteins; C116005:Ran binding protein 9; D014409:Tumor Necrosis Factor-alpha; C000606291:Sod1 protein, mouse; D013482:Superoxide Dismutase; D000072105:Superoxide Dismutase-1; D051058:Oncogene Protein v-akt; D048049:Extracellular Signal-Regulated MAP Kinases; D020744:rac GTP-Binding Proteins