Department of Standard Research, Korea Institute of Oriental Medicine, Daejeon, Korea.
Neurodegener Dis. 2011;8(6):504-14. doi: 10.1159/000327911. Epub 2011 Aug 18.
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.
由于肌萎缩侧索硬化症（ALS）是一种进行性炎症性疾病，因此治疗肺部系统在 ALS 患者的护理中起着关键作用。以前的研究主要检查了中枢神经系统中 ALS 的病理机制；然而，对于 ALS 动物模型中的肺部系统，研究相对较少。在包括哮喘和关节炎在内的炎症性疾病中，电针（EA）通常因其抗炎作用而被使用。本研究的目的是确定 EA 治疗是否会影响 ALS 动物模型中的肺部系统炎症。
在 14 周龄的 hSOD1（G93A）转基因小鼠中进行 ST36（足三里）穴位的 EA 治疗。使用抗离子钙结合衔接分子 1（Iba-1）和抗肿瘤坏死因子 α（TNF-α）抗体进行免疫组织化学分析。为了研究炎症蛋白的表达水平，使用抗 Iba-1、抗 TNF-α、抗核因子 kappa B（NF-κB）和抗白细胞介素 6（IL-6）抗体进行 Western blot 分析。还通过 Western blot 评估了 EA 处理和未处理的 hSOD1（G93A）小鼠肺组织中 Ser435-磷酸化特异性 RAC-α丝氨酸/苏氨酸蛋白激酶 1（pAKT）的激活和磷酸化细胞外信号调节激酶（pERK）蛋白的增加。
与对照 hSOD1（G93A）小鼠相比，EA 治疗降低了促炎蛋白如 TNF-α和 IL-6、pNF-κB 和 Iba-1 的表达，并增加了激活的 pAKT 和 pERK 的水平。
我们的研究结果表明，EA 可能是治疗 ALS 动物模型中呼吸功能障碍的有效抗炎治疗方法。
