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Anti-inflammatory Effect of an Ethanolic Extract of Myagropsis yendoi in Lipopolysaccharide-Stimulated BV-2 Microglia Cells

机译:脂多糖刺激的BV-2小胶质细胞对肌无肌症的乙醇提取物的抗炎作用。

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摘要

Marine brown algae have been identified as a rich source of structurally diverse bioactive compounds. Whether Myagropsis yendoi ethanolic extracts (MYE) inhibit inflammatory responses was investigated using lipopolysaccharide (LPS)-stimulated microglia BV-2 cells. MYE inhibited LPS-induced nitric oxide (NO) production in a dose-dependent manner and suppressed the expression of inducible nitric oxide synthase in BV-2 cells. MYE also reduced the production of pro-inflammatory cytokines in LPS-stimulated BV-2 cells. LPS-induced nuclear factor-icB (NF-kB) transcriptional activity and NF-kB translocation into the nucleus were significantly inhibited by MYE treatment through preventing degradation of the inhibitor kB-cl Moreover, MYE inhibited the phosphorylation of AK.T, ERK, JNK, and p38 mitogen-activated protein kinase in LPS-stimulated BV-2 cells. These results indicate that MYE is a potential source of therapeutic or functional agents for neuroinflammatory diseases.
机译:海洋褐藻已被确认为结构多样的生物活性化合物的丰富来源。使用脂多糖(LPS)刺激的小胶质细胞BV-2细胞研究了Myagropsis yendoi乙醇提取物(MYE)是否抑制炎症反应。 MYE以剂量依赖的方式抑制LPS诱导的一氧化氮(NO)的产生,并抑制BV-2细胞中诱导型一氧化氮合酶的表达。 MYE还减少了LPS刺激的BV-2细胞中促炎性细胞因子的产生。通过MYE处理,通过防止抑制剂kB-cl的降解,LPS诱导的核因子-icB(NF-kB)转录活性和NF-kB易位进入核内。此外,MYE抑制AK.T,ERK, LPS刺激的BV-2细胞中的JNK和p38丝裂原激活的蛋白激酶。这些结果表明,MYE是神经炎性疾病的治疗或功能药物的潜在来源。

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