A TNF-α blocking peptide that reduces NF-κB and MAPK activity for attenuating inflammation

[Display omitted] 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,...

Full description

Saved in:
Bibliographic Details
Published in:Bioorganic & medicinal chemistry 2023-09, Vol.92, p.117420-117420, Article 117420
Main Authors: Wang, Yue, Ye, Ruiwei, Fan, Liming, Zhao, Xin, Li, Linxue, Zheng, Hao, Qiu, Yan, He, Xiuxia, Lu, Yiming
Format: Article
Language:English
Subjects:
Inflammation
Molecular docking
Peptide
TNF-α
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:[Display omitted] 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.
ISSN:0968-0896
1464-3391
DOI:10.1016/j.bmc.2023.117420