S‐allyl cysteine inhibits TNF‐α‐induced inflammation in HaCaT keratinocytes by inhibition of NF‐ κB‐dependent gene expression via sustained ERK activation

• DOI: 10.1111/exd.14041
• Publication Date: 2019-09-19T11:43:30Z
• Authors: Chitra Basu; Abhipriya Chatterjee; Sampurna Bhattach...; Naibedya Dutta; Runa Sur
• Keywords: HaCaT; Proinflammatory cytokine

Abstract Tumor necrosis factor‐α (TNF‐α)‐induced keratinocyte inflammation plays a key role in the pathogenesis of multiple inflammatory skin diseases. Here we investigated anti‐inflammatory effect S‐allyl cysteine (SAC) on TNF‐α‐induced HaCaT cells and mechanism behind its potential. SAC was found to inhibit TNF‐α‐stimulated cytokine expression. Further, activation p38, JNK NF‐κB pathways. Interestingly, differentially regulate ERK MAP kinase cells. transient treatment resulted sustained both presence absence TNF‐α. Additionally, failed expression pro‐inflammatory cytokines TNF‐α IL‐1β when were treated with MEK inhibitor PD98059, suggesting that is via pathway. Since has been reported negatively NF‐κB‐driven gene find activates regulates NF‐κB, whether there existed any crosstalk between NF‐κB‐dependent reporter assay, visualization nuclear translocation NF‐κB‐p65 subunit determination cellular levels I‐κB, revealed inhibited activation, PD98059 reversed this effect. These results collectively suggest inhibits combined entailing inhibition p38 pathways pathway ERK.