Department of Neurology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, 050000, China.
Key Laboratory of Hebei Neurology, Shijiazhuang, Hebei, 050000, China.
IUBMB Life. 2018 May;70(5):432-436. doi: 10.1002/iub.1739. Epub 2018 Apr 10.
Multiple sclerosis (MS) is a poorly understood disease mechanistically. MOG35-55 peptide induced experimental autoimmune encephalomyelitis (EAE) is a broadly used model to study MS. Using this model we have earlier shown that the antioxidant tempol or the small molecule inhibitor of p38 SB203580 can effectively prevent EAE progression. This effect was mediated by means of regulating immune inflammation, signaling by the p38MAPK-SGK1 pathway, and oxidative stress. However, there is a need to test drugs that can be used in pharmacological intervention of EAE. Given that nordihydroguaiaretic Acid (NDGA) has been shown to possess anti-oxidant activity and capacity of antagonizing autoimmune inflammation, we tested the effect of NDGA in ameliorating EAE in the current study. NDGA showed significant beneficial effect against EAE with both anti-inflammation and antioxidant activity. NDGA could weaken the immune inflammation at least partly by inhibiting the oxidant stress-p38MAPK-SGK1 pathway representing a target for putative pharmacological intervention. © 2018 IUBMB Life, 70(5):432-436, 2018.
多发性硬化症（MS）在机制上是一种难以理解的疾病。MOG35-55 肽诱导的实验性自身免疫性脑脊髓炎（EAE）是一种广泛用于研究 MS 的模型。使用该模型，我们之前已经表明，抗氧化剂替普洛尔或 p38MAPK-SGK1 通路的小分子抑制剂 SB203580 可以有效预防 EAE 进展。这种作用是通过调节免疫炎症、p38MAPK-SGK1 通路的信号转导和氧化应激来介导的。然而，需要测试可用于 EAE 药理干预的药物。鉴于已显示去甲二氢愈创木酸（NDGA）具有抗氧化活性和拮抗自身免疫炎症的能力，我们在本研究中测试了 NDGA 改善 EAE 的效果。NDGA 对 EAE 具有显著的抗炎和抗氧化作用。NDGA 可以通过抑制氧化应激-p38MAPK-SGK1 通路来减弱免疫炎症，这代表了潜在的药理干预的靶点。
