Ward Thirty-Three, Department of Emergency Cardiology, Beijing Anzhen Hospital, Capital Medical University, Beijing 100029, China.
The MOH Key Laboratory of Geriatrics, Beijing Hospital, National Center of Gerontology, Beijing 100730, China.
Anal Cell Pathol (Amst). 2018 May 2;2018:5762371. doi: 10.1155/2018/5762371. eCollection 2018.
To investigate the function of polysaccharides (TFPS) in LPS-induced inflammation and oxidative stress of macrophages.
RAW264.7 cells were pretreated with TFPS and then stimulated with 0.1 g/ml LPS. NFB, Akt, p38MAPK, MCP-1, and SOD-1 were analyzed by Western blotting. Cell viability was measured using MTT assays. Reactive oxygen species (ROS) production, real-time PCR, ELISA, and immunofluorescence staining were performed on RAW264.7 cells that were treated with LPS and/or TFPS to investigate the anti-inflammatory effect of TFPS.
LPS induced inflammation and ROS production and promoted the secretion of cytokines such as TNF- and IL-6. LPS also enhanced the nuclear translocation of NFB, which promoted inflammation by oxidative stress. However, pretreatment with TFPS profoundly inhibited the activation of Akt, p38MAPK, and NFB and attenuated the expression of MCP-1 in macrophages. Meanwhile, TFPS also decreased cytokine and ROS levels and attenuated cell inflammation after treatment with LPS. Moreover, miR-155, one of the key small RNAs which regulate NFB and inflammation in macrophages, was significantly downregulated.
TFPS inhibits LPS-induced oxidative stress and inflammation by inhibiting miR-155 expression and NFB activation in macrophages, which suggests that TFPS may be a potential reagent for inhibiting the development of inflammation.
研究多糖（TFPS）在 LPS 诱导的巨噬细胞炎症和氧化应激中的作用。
用 TFPS 预处理 RAW264.7 细胞，然后用 0.1μg/ml LPS 刺激。用 Western blot 分析 NFB、Akt、p38MAPK、MCP-1 和 SOD-1。用 MTT 法测定细胞活力。用 LPS 和/或 TFPS 处理 RAW264.7 细胞，进行活性氧（ROS）产生、实时 PCR、ELISA 和免疫荧光染色，以研究 TFPS 的抗炎作用。
LPS 诱导炎症和 ROS 产生，并促进 TNF-α和 IL-6 等细胞因子的分泌。LPS 还增强了 NFB 的核转位，通过氧化应激促进炎症。然而，TFPS 预处理可显著抑制 Akt、p38MAPK 和 NFB 的激活，并减弱巨噬细胞中 MCP-1 的表达。同时，TFPS 还降低了 LPS 处理后的细胞因子和 ROS 水平，并减轻了细胞炎症。此外，miR-155 是调节巨噬细胞中 NFB 和炎症的关键小 RNA 之一，其表达显著下调。
TFPS 通过抑制 miR-155 表达和 NFB 激活来抑制 LPS 诱导的氧化应激和炎症，这表明 TFPS 可能是抑制炎症发展的潜在试剂。
