Suppression of infection-induced endotoxin shock in mice by a Citrus flavanone naringin
Suppression of infection-induced endotoxin shock in mice by a Citrus flavanone naringin
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DOI：
10.1055/s-2004-815449
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发表时间：
2004-01-01
期刊：
影响因子：
2.7
通讯作者：
Kumazawa, Y
中科院分区：
文献类型：
--
作者：
Kawaguchi, K;Kikuchi, S;Kumazawa, Y
柑橘黄烷酮柚皮苷的保护作用在基于沙门氏菌感染的内毒素休克模型中得到了证明。腹膜内 (i.p.) 感染 10(8) CFU 鼠伤寒沙门氏菌 aroA 会导致脂多糖 (LPS) 应答小鼠出现致命性休克，但不会对 LPS 无应答小鼠造成致命性休克。感染前 3 小时给予 1 mg 柚皮苷可防止致命性休克，与 LPS 无反应小鼠类似。柚皮苷的保护作用具有时间和剂量依赖性。柚皮苷治疗不仅导致脾脏和肝脏中的细菌数量显着减少，而且还导致血浆脂多糖水平降低。此外，柚皮苷显着抑制TNF-α并使感染引起的凝血因子的激活状态正常化，例如凝血酶原时间、纤维蛋白原浓度和血小板数量。有趣的是，柚皮苷治疗抑制了感染引起的高水平可溶性 CD14 和高迁移率 1 族分子。
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.