Microglial inflammation plays an essential role in neurodegenerative disease. Our previous studies had shown that κ-carrageenan oligosaccharides (KOS) could inhibit the excessive activation of microglia that induced by LPS, while the interrelated mechanisms were still indistinct. Therefore, we detected the inflammatory signaling pathway on LPS-activated microglia that pretreat by different content of KOS to reveal the mechanism on KOS's inhibition of microglia inflammatory response. ELISA was used to detect the effects of KOS on the secretion of interleukin-1 (IL-1β), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and prostaglandin E2 (PG-2) by LPS-activated microglia, respectively. The production of reactive oxygen species (ROS) and nitric oxide (NO) in microglia cells was detected by flow cytometry, and the protein expression of immunoinflammation-related signaling pathways were detected by Western Blot. The results showed that KOS could significantly protected the microglia from the over-activated inflammatory by inhibiting the release of inflammatory cytokines and the oxidative stress response. And KOS could reduce the expression of the protein that related to the TLR4/NF-κB and p38/JNK MAPKs pathways activated by LPS in microglia. However, there may be no specific target of KOS in cells. Therefore, KOS, a natural algal source oligosaccharide, has immunomodulatory effects and can be used as a potential intervention therapy for inflammatory related neurodegenerative diseases.

小胶质细胞炎症在神经退行性疾病中起重要作用。我们之前的研究表明，κ-卡拉胶寡糖（KOS）可以抑制LPS诱导的小胶质细胞过度活化，但相关机制尚不明确。因此，我们检测了不同含量的KOS预处理后LPS激活的小胶质细胞的炎症信号通路，揭示了KOS抑制小胶质细胞炎症反应的机制。ELISA法检测KOS对白细胞介素1（IL-1β）、肿瘤坏死因子α（TNF-α）、白细胞介素6（IL-6）和前列腺素E2（PG-2）分泌的影响。 LPS 激活的小胶质细胞，分别。流式细胞仪检测小胶质细胞中活性氧（ROS）和一氧化氮（NO）的产生，Western Blot检测免疫炎症相关信号通路的蛋白表达。结果表明，KOS可通过抑制炎性细胞因子的释放和氧化应激反应，显着保护小胶质细胞免受过度激活的炎症反应。并且KOS可以降低小胶质细胞中LPS激活的TLR4/NF-κB和p38/JNK MAPKs通路相关蛋白的表达。然而，细胞中可能没有特定的 KOS 靶点。因此，天然藻源寡糖KOS具有免疫调节作用，可作为炎症相关神经退行性疾病的潜在干预疗法。结果表明，KOS可通过抑制炎性细胞因子的释放和氧化应激反应，显着保护小胶质细胞免受过度激活的炎症反应。并且KOS可以降低小胶质细胞中LPS激活的TLR4/NF-κB和p38/JNK MAPKs通路相关蛋白的表达。然而，细胞中可能没有特定的 KOS 靶点。因此，天然藻源寡糖KOS具有免疫调节作用，可作为炎症相关神经退行性疾病的潜在干预疗法。结果表明，KOS可通过抑制炎性细胞因子的释放和氧化应激反应，显着保护小胶质细胞免受过度激活的炎症反应。并且KOS可以降低小胶质细胞中LPS激活的TLR4/NF-κB和p38/JNK MAPKs通路相关蛋白的表达。然而，细胞中可能没有特定的 KOS 靶点。因此，天然藻源寡糖KOS具有免疫调节作用，可作为炎症相关神经退行性疾病的潜在干预疗法。细胞中可能没有特定的 KOS 靶点。因此，天然藻源寡糖KOS具有免疫调节作用，可作为炎症相关神经退行性疾病的潜在干预疗法。细胞中可能没有特定的 KOS 靶点。因此，天然藻源寡糖KOS具有免疫调节作用，可作为炎症相关神经退行性疾病的潜在干预疗法。