Neuro-degenerative diseases · 2011
Anti-inflammatory effects of electroacupuncture in the respiratory system of a symptomatic amyotrophic lateral sclerosis animal model.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Jiang Jing Hua, Yang Eun Jin, Baek Myung Gi, Kim Seon Hwy, Lee Sang Min, Choi Sun-Mi
Аннотация
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.
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.
Предметные рубрики MeSH
Adaptor Proteins, Signal TransducingAmyotrophic Lateral SclerosisAnimalsBlotting, WesternCell CountCell SurvivalCytoskeletal ProteinsElectroacupunctureExtracellular Signal-Regulated MAP KinasesFemaleImmunohistochemistryInflammationInterleukin-6LungMaleMiceMice, TransgenicNF-kappa BNuclear ProteinsOncogene Protein v-aktRespiratory Tract DiseasesSuperoxide DismutaseSuperoxide Dismutase-1Tumor Necrosis Factor-alpharac GTP-Binding Proteins