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A Citrus Flavonoid Hesperidin Suppresses Infection-Induced Endotoxin Shock in Mice

机译:柑橘类黄酮橙皮苷抑制小鼠感染引起的内毒素休克。

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Administration of a citrus flavonoid hesperidin (HES) to mice before LPS challenge significantly reduced tumor necrosis factor (TNF)-α production in a dose-dependent manner. Treatment of HES 3 h before intraperitoneal (i.p.) infection with 10~8 CFU Salmonella typhimurium aroA resulted in rescue from lethal shock as similar to LPS-nonresponder mice. Not only bacterial numbers in livers and spleens but also plasma LPS levels significantly decreased by pretreatment with HES. In addition, HES markedly suppressed plasma levels of TNF-α and high mobility group box chromosomal protein 1 (HMGB-1), decreased the number of apoptotic cells in livers and normalized the activated states of blood coagulation factors such as prothrombin time and platelet numbers caused by infection. Pretreatment of LPS with HES suppressed the chromogenic Limulus reaction.
机译:在LPS攻击前向小鼠施用柑桔类黄酮橙皮苷(HES),以剂量依赖的方式显着降低了肿瘤坏死因子(TNF)-α的产生。与LPS无反应小鼠相似,用10〜8 CFU鼠伤寒沙门氏菌aroA腹膜内(i.p.)感染HES进行治疗3小时。通过HES预处理,不仅肝脏和脾脏中的细菌数量显着降低,而且血浆LPS水平也显着降低。此外,HES显着抑制了血浆中的TNF-α和高迁移率族盒染色体蛋白1(HMGB-1)的水平,减少了肝脏中凋亡细胞的数量,并使凝血因子的激活状态(如凝血酶原时间和血小板数量)正常化。由感染引起。用HES预处理LPS可抑制发色Li反应。

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