OBJECTIVE

has been reported for its anti-inflammatory properties. However, its efficacy in sepsis has yet to be reported. In this study, we studied the ability of extract (DIE) to rescue mice from septic shock and sepsis.

METHODS

studies included the measurement of secreted nitric oxide, cell viability, gene and protein expression via real-time polymerase chain reaction and western blot, and confocal microscopy in RAW 264.7 cells. studies include a model of septic shock and sepsis in BALB/c mice induced by a lethal and sub-lethal dose of lipopolysaccharide (LPS).

RESULTS

DIE suppressed the expression of proinflammatory cytokines induced by LPS and prevented the translocation of NFB into the nucleus of RAW 264.7 cells. It also prevented reactive oxygen species damage induced by LPS in murine bone marrow-derived macrophages. Models of sepsis and septic shock were established in BALB/ mice and DIE-rescued mice from septic shock. DIE also reversed the increase in tumor necrosis factor- and nitrite levels in the serum of mice induced with sepsis. DIE also prevented the translocation of NFB from the cytosol into the nucleus in murine lungs. Histopathological damage induced by sepsis was reversed in the testis, liver, and lungs of mice.

CONCLUSION

In conclusion, DIE is a suitable candidate for development as a therapeutic agent for sepsis.