Benzylurea

Benzylurea is an anti-inflammatory agent. Benzylurea inhibits LPS (HY-D1056)-induced upregulation of MTCH2 expression and regulates pathways associated with mitochondrial function, inflammation and cell survival. Benzylurea alleviates LPS-induced proliferation inhibition and apoptosis of periodontal ligament fibroblasts, as well as the release of proinflammatory cytokines. Benzylurea can be used in studies related to periodontitis^[1]. In Vitro:Benzylurea (0-120 μM; 24 h) protects human periodontal ligament fibroblasts (hPDLFs) against LPS (HY-D1056)-induced loss of viability, and exhibits low intrinsic cytotoxicity to hPDLFs at the concentration of 10 μM; whereas higher concentrations (20-120 μM; 24 h) reduce the viability of hPDLFs in a dose-dependent manner^[1].
Benzylurea (10 μM; 24 h) inhibits the secretion of IL-1β, IL-6 and TNF-α induced by LPS in human periodontal ligament fibroblasts (hPDLFs), and blocks the nuclear translocation of NF-κB p65^[1].
Benzylurea (10 μM; 24 h) restores the mitochondrial membrane potential of human periodontal ligament fibroblasts (hPDLFs) damaged by LPS and inhibits the production of ROS^[1].
Benzylurea (10 μM; 24 h) can restructure and restore the F-actin cytoskeleton in human periodontal ligament fibroblasts (hPDLFs) damaged by LPS^[1].
Benzylurea (10 μM; 24 h) regulates protein expression in hPDLFs by reducing LPS-induced levels of MTCH2, NF-κB p65, Bax, IL-1β, IL-8 and NLRP3, while increasing the LPS-suppressed levels of CYB5B and BCL2^[1].