Suppression of infection-induced endotoxin shock in mice by a citrus flavanone naringin.
The protective effect of the Citrus flavanone naringin was demonstrated in an endotoxin shock model based on Salmonella infection. Intraperitoneal ( i. p.) infection with 10 (8) CFU Salmonella typhimurium aroA caused lethal shock in lipopolysaccharide (LPS) -responder but not LPS-non-responder mice. Administration of 1 mg naringin 3 h before infection resulted in protection from lethal shock, similar to LPS-non-responder mice. The protective effect of naringin was time- and dose-dependent. Treatment with naringin resulted not only in a significant decrease in bacterial numbers in spleens and livers, but also in a decrease in plasma LPS levels. In addition, naringin markedly suppressed TNF-alpha and normalized the activated states of blood coagulation factors such as prothrombin time, fibrinogen concentration and platelet numbers caused by infection. Interestingly, treatment with naringin suppressed high levels of soluble CD14 and high mobility group-1 molecule caused by infection.[1]References
- Suppression of infection-induced endotoxin shock in mice by a citrus flavanone naringin. Kawaguchi, K., Kikuchi, S., Hasunuma, R., Maruyama, H., Ryll, R., Kumazawa, Y. Planta Med. (2004) [Pubmed]
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