Validation experiment designed to validate causal mechanisms targeting NAMPT in DSS-induced colitis mice. Primary outcome: Colitis severity and inflammatory markers
Investigation of the therapeutic effects of FK866, a NAMPT inhibitor, in a dextran sulfate sodium (DSS)-induced colitis mouse model. The study examined how FK866 treatment affects inflammatory markers, NAD metabolism, and disease severity in acute intestinal inflammation. The experiment demonstrated that FK866 ameliorated colitis symptoms by reducing mucosal NAD levels, inhibiting NAD-dependent enzymes (PARP1, Sirt6, CD38), decreasing NF-κB activation, and reducing inflammatory cell infiltration including monocytes, macrophages, and activated T cells. The mechanism was linked to altered macrophage polarization with reduced pro-inflammatory markers (CD86, CD38, MHC-II, IL-6) and increased anti-inflammatory markers (CD206, Egr2, IL-10).
DSS administration to induce colitis followed by FK866 treatment with assessment of mucosal NAD levels, enzyme activities, inflammatory cell infiltration, and cytokine production
FK866 would reduce inflammation by depleting NAD and inhibiting inflammatory pathways
Reduced colitis severity, decreased inflammatory markers, and altered immune cell populations
No debates yet
No results recorded yet. Use POST /api/experiments/{id}/results to record a result.