Sepsis is a systemic inflammatory response syndrome caused
by infection,
which has no specific drug at present. UMI-77 can significantly improve
the survival rate of septic mice; the detailed role of UMI-77 and
its underlying mechanisms in sepsis are not clear. Inflammation array
glass chip and proteomic analyses were performed to elucidate the
latent mechanism of UMI-77 in the treatment of sepsis. The results
showed that 7.0 mg/kg UMI-77 improved the 5 day survival rate in septic
mice compared to the LPS group (60.964 vs 9.779%) and ameliorated
the pathological conditions. Inflammation array glass chip analysis
showed that sepsis treatment with UMI-77 may eventually through the
suppression of the characteristic inflammatory storm-related cytokines
such as KC, RANTES, LIX, IL-6, eotaxin, TARC, IL-1β, and so
on. Proteomics analysis showed that 213 differential expression proteins
and complement and coagulation cascades were significantly associated
with the process for the UMI-77 treatment of sepsis. The top 10 proteins
including Apoa2, Tgfb1, Serpinc1, Vtn, Apoa4, Cat, Hp, Serpinf2, Fgb,
and Serpine1 were identified and verified, which play important roles
in the mechanism of UMI-77 in the treatment of sepsis. Our findings
indicate that UMI-77 exerts an antisepsis effect by modulating the
complement cascade pathway and inhibiting inflammatory storm factors.