RESUMEN
In the present study, the dual function of interleukin-23 (IL-23) Aptamer to suppress brain inflammation via attachment to macrophage stimulating 1 (MST1) kinase and IL-23, was introduced. Also, the anti-inflammatory property of IL-23 Aptamer has been investigated. This study showed that IL-23 Aptamer could reduce the clinical development of brain inflammation induced by Parathion, as an important organophosphate toxin. Both immunostaining and H&E staining indicated that the total inflammatory infiltration foci were remarkably decreased in IL-23 Aptamer-treated mice. Moreover, this study showed that IL-23 Aptamer reduced both absolute and relative numbers of MST1+CD4â¯+â¯Th1 cells and IL-23-producing cells. Analysis of the Hippo signaling genes showed a sharp decrease of MST1 kinase compared with other genes (Pâ¯<â¯0.001). Moreover, computer-assisted molecular docking demonstrated that both MST1 kinase and IL-23 could tightly attach to IL-23 Aptamer, and maybe block it. Taken together, IL-23 Aptamer coud decrease brain inflammation via suppressing MST1 kinase and IL-23.