Chronic inflammation is a pivotal event in the pathogenesis of cardiovascular diseases, including atherosclerosis, restenosis, and coronary artery disease. The efficacy of current treatment or preventive strategies for such inflammation is still inadequate. Thus, new anti-inflammatory strategies are needed. TNF-α, IL-1β, and IL-6 are common pro-inflammatory cytokines. It was shown that TNF-α and IL-1β expression levels dramatically increase in the early stage of sepsis. In addition, studies have shown that the concentration of IL-6 in blood was related with severe sepsis. Therefore, it is possible to understand the severity of sepsis by detecting TNF-α, IL-1β and IL-6 and to provide a new treatment method by inhibiting TNF-α, IL- 1β, and IL-6 syntheses and their signal transductions to reduce inflammation. In this study, we designed and synthesized inhibitory peptides based on in silico investigations into the pro-inflammatory cytokines-receptors bindings which link to sepsis. The anti-inflammatory potential of the de novo designed peptides was tested in human micro-vascular endothelial cell-1 treated with pro-inflammatory cytokines, such as TNF-α, IL-1β and IL-6. The p65 translocation was investigated by luciferase assay and immunofluorescence. According to our data, TNF-α induced p65 translocation was decreased by peptide treatment. However, no significant differences were observed in vehicles or IL-1β, IL-6-induced groups. In the current study, we found that de novo peptide had partial anti-inflammatory ability in the presence of TNF-α-induced inflammation, whereas there was no significant difference in IL-1β, and IL-6-induced inflammation.

Potential peptide based on in silico analysis can bind proinflammatory cytokines as a therapeutic strategy for anti-inflammation

256th National Meeting (2018)

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