| Summary: | 碩士 === 臺北醫學大學 === 醫學科學研究所 === 102 === Circulation monocytes can be recuited to the infected or injured tissue and differentiate into macrophages or dendritic cells. In many documents, blood monocytes can be stimulated and secrete cytokines which regulate immune
function or cause inflammation. LPS can induce the experssion of many pro-inflammatory mediators in human monocytes, such as TNF-α、IL-6 and IL-1β, play important roles in sepsis or chronic infection. These cytokines
could also enhance the proteinase. (such as matrix metalloproteinase-9) production in monocytes, which leads to serious tissue injury. Theissenolactone C (LC53) is derived from the Taiwan strains Xylariaceae (Xylariaceae) Theissenia cinerea. We found LC53 obviously decrease LPS-induced extracellular MMP-9, TNF-α and IL-6 expression in THP-1 cells within 24 hours. It also inhibits LPS-induced extracellular MMP-9 protein and mRNA expression. In signaling studies, LC53 could block the LPS-induced degradation of IκBα, p65 translocation, and NF-κB regulated gene reporter activity . It also decreased the phosphorylation of IKKα/β while not affected the p38 phosphorylation. Consistently, after LC53 treatment, the NF-κB signaling and IPA-related gene network of MMP-9 was apparently interacted by microarray analyses. It will be interesting to evaluate the therapeutic potential of LC53 in animal septic model.
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