Abstract
Sepsis is a major health threat that remains refractory to treatment. Impairment of normal cellular function due to oxidative stress is implicated in organ injury during systemic inflammatory responses. We investigated whether the new anti-oxidative drug, ETS-GS, could inhibit secretion of cytokines and mono-nitrogen oxides, thus reducing organ damage in a rat model of lipopolysaccharide-induced sepsis. Lipopolysaccharide was administered intravenously to male Wistar rats in order to establish a rat model of systemic inflammation. These rats were challenged with or without intravenous ETS-GS. Mouse macrophage RAW264.7 cells were stimulated with lipopolysaccharide, with or without simultaneous ETS-GS treatment, in order to elucidate the mechanism of action. Histologic examination revealed that ETS-GS markedly reduced lipopolysaccharide-induced interstitial edema and leukocytic infiltration in lung tissue, and lipopolysaccharide-induced bleeding and leukocytic infiltration in liver tissue harvested 12 h after treatment. Cytokine (interleukin-6 and tumor necrosis factor-α) secretion was strongly induced by lipopolysaccharide; this induction was similarly inhibited by ETS-GS treatment. Likewise, lipopolysaccharide-induced secretion...Continue Reading
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