Thymoquinone reduces mortality and suppresses early acute inflammatory markers of sepsis in a mouse model.

BACKGROUND

Sepsis is a severe systemic condition caused by an excessive inflammatory response to microbial infections, which often results in high mortality.

AIMS

In the present study, the therapeutic effects of thymoquinone were investigated for Gram-negative bacteria-induced sepsis in mice.

METHODS

Thymoquinone was administered as 1or 2?mg/kg intraperitoneally 2?h after Escherichia coli (E. coli) challenge. Animal morality was assessed up to 96?h post infection and inflammatory proteins levels were measured 6?h after thymoquinone treatment in various groups using enzyme-linked immunosorbent assay (ELISA) techniques.

KEY FINDINGS

The E. coli inoculation markedly increased the level of plasma cytokines, including tumor necrosis factor (TNF)-?, interleukin (IL)-1, IL-2, IL-6 and IL-10. In addition, the levels of selected early sepsis biomarkers such as CRP, VEGF and ESM-1 were amplified in the septic group. Treatment with thymoquinone significantly downregulated the circulating concentrations of the inflammatory proteins (p?<?0.05). In addition, ?75% of mice in the thymoquinone (1?mg/kg) group survived at 96h of observation compared with ?8% of the untreated group (p?=?0.0016).

SIGNIFICANCE

The present results indicate that thymoquinone suppresses acute inflammatory responses induced by sepsis including early stage biomarkers and reduces sepsis-related mortality. These findings suggest that thymoquinone could be of a potential therapeutic value in the management of sepsis.