一种 TNF-α 阻断肽，可减少 NF-κB 和 MAPK 活性，从而减轻炎症。
A TNF-α blocking peptide that reduces NF-κB and MAPK activity for attenuating inflammation.
机构信息
School of Life Science and Technology, Changchun University of Science and Technology, Changchun 130013, China.
School of Medicine, Shanghai University, Shanghai 200444, China.
出版信息
Bioorg Med Chem. 2023 Sep 7;92:117420. doi: 10.1016/j.bmc.2023.117420. Epub 2023 Jul 20.
Overexpression of tumor necrosis factor-α (TNF-α) is implicated in many inflammatory diseases, including septic shock, hepatitis, asthma, insulin resistance and autoimmune diseases, such as rheumatoid arthritis and Crohn's disease. The TNF-α signaling pathway is a valuable target, and anti-TNF-α drugs are successfully used to treat autoimmune and inflammatory diseases. Here, we study anti-inflammatory activity of an anti-TNF-α peptide (SN1-13, DEFHLELHLYQSW). In the cellular level assessment, SN1-13 inhibited TNF-α-induced cytotoxicity and blocks TNF-α-triggered signaling activities (IC50 = 15.40 μM). Moreover, the potential binding model between SN1-13 and TNF-α/TNFRs conducted through molecular docking revealed that SN1-13 could stunt TNF-α mediated signaling thought blocking TNF-α and its receptor TNFR1 and TNFR2. These results suggest that SN1-13 would be a potential lead peptide to treat TNF-α-mediated inflammatory diseases.
肿瘤坏死因子-α（TNF-α）的过表达与许多炎症性疾病有关，包括感染性休克、肝炎、哮喘、胰岛素抵抗和自身免疫性疾病，如类风湿关节炎和克罗恩病。TNF-α 信号通路是一个有价值的靶点，抗 TNF-α 药物成功地用于治疗自身免疫和炎症性疾病。在这里，我们研究了一种抗 TNF-α 肽（SN1-13，DEFHLELHLYQSW）的抗炎活性。在细胞水平评估中，SN1-13 抑制 TNF-α 诱导的细胞毒性并阻断 TNF-α 触发的信号活性（IC50 = 15.40 μM）。此外，通过分子对接进行的 SN1-13 与 TNF-α/TNFRs 之间的潜在结合模型表明，SN1-13 可以通过阻断 TNF-α及其受体 TNFR1 和 TNFR2 来阻碍 TNF-α 介导的信号转导。这些结果表明，SN1-13 可能成为治疗 TNF-α 介导的炎症性疾病的潜在先导肽。
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