Anti-Inflammatory Effects of Electroacupuncture in the Respiratory System of a Symptomatic Amyotrophic Lateral Sclerosis Animal Model

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 rela...

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Veröffentlicht in:Neuro-degenerative diseases 2011-01, Vol.8 (6), p.504-514
Hauptverfasser: Jiang, Jing Hua, Yang, Eun Jin, Baek, Myung Gi, Kim, Seon Hwy, Lee, Sang Min, Choi, Sun-Mi
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Sprache:eng
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Zusammenfassung: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-ĸB), 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-ĸB, 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.
ISSN:1660-2854
1660-2862
DOI:10.1159/000327911