Effects of a synthetic di‐phosphoserine peptide (SS‐2) on gene expression profiling against TNF‐α induced inflammation. (8th January 2019)

• Record Type: Journal Article
• Authors: Zhang, Hua; Xu, Cai Na; Mine, Yoshinori
• Is Part Of: International journal of food science & technology. Volume 54:Number 6(2019)
• Page Start: 2010
• Page End: 2020
• Publication Date: 2019-01-08
• Subjects: Anti‐inflammatory activity -- cell signalling pathway -- di‐phosphoserine peptide -- mitogen‐activated protein kinase -- nuclear factor‐kappa B; Food industry and trade -- Periodicals; 664
• DOI: 10.1111/ijfs.14077
• Languages: English
• ISSNs: 0950-5423

Abstract

Summary: It has been showed bioactive di‐phosphoserine peptide (SS‐2) possesses functions to ameliorate oxidative stress in vitro . This study aimed to substantiate the role of bioactive di‐phosphoserine peptide (SS‐2) in modulating inflammatory responses in TNF‐α‐stimulated HT‐29 cells, and its mechanism of action. SS‐2 significantly reduced IL‐8 secretion in TNF‐α‐induced HT‐29 cells, and also suppressed pro‐inflammatory cytokines, including IL‐8, IL‐12, MCP‐1 and TNF‐α. Moreover, SS‐2 inhibited TNF‐α initiated signalling cascades by suppressing phosphorylation of the ERK1/2, JNK, P38 and IκB those culminate in above cellular inflammatory responses. Differentially expressed genes analysis within NF‐κB signalling pathway revealed that SS‐2 blocks multiple sites of upstream NF‐κB signalling cascade, including FADD and MyD88, thereby preventing the signalling transduction involved in cellular inflammatory response. These results provide a new insight into molecular mechanism for anti‐inflammatory action of SS‐2, suggesting SS‐2 is a potential alternative approach to treat IBD by particular targeting TNF‐α driven inflammatory event. Abstract : Di‐phosphoserine peptide inhibits TNF‐α initiated signalling cascades by suppressing phosphorylation of the ERK1/2, JNK, P38 and I&kgr;B . Di phosphoserine peptide blocks multiple sites of upstream NF‐&kgr;B signalling cascade.