Zuo Dan, Zhou Wang-mei, Guo Bing-bing, Mei Gui-ping
Nursing Department, General Hospital of Guangzhou Command, Guangzhou 510010, China.
Nan Fang Yi Ke Da Xue Xue Bao. 2010 Feb;30(2):263-5.
To investigate the effects of co-exposure to hyperthermia and lipopolysaccharides (LPS) on tumor necrosis factor-alpha (TNF-alpha) expression in the lungs and small intestines of rats.
Male pathogen-free Wistar rats were randomly assigned into saline-injected normothermic control (C), saline heat exposure (H), LPS normothermic control (L), and LPS plus heat exposure (HL) groups. The rats in H and HL groups were exposed in a chamber at an ambient dry bulb temperature (Tdb) of 35.0-/+0.5 degrees celsius;, and those in C and L groups to 26-/+0.5 degrees celsius;. In L and HL groups, the rats were given an intravenous injection of LPS 10 mg/kg via the tail vein to induce endotoxemia, and those in C and H group received 10 ml/kg injection. The plasma levels of sTNFrI and sTNFrII were detected at different time points using ELISA. The expression of TNF-alpha in the lungs and small intestines was detected by immunohistochemical SABC method, and the damage of the lungs and small intestines evaluated histologically 120 min after the treatment.
Co-exposure to hyperthermia and LPS caused significantly enhanced expressions of TNF-alpha and its receptor sTNFrI and sTNFrII in the plasma and tissues and obvious histopathological damage in the lung and small intestines.
Co-stress of hyperthermia and LPS-induced toxicity is associated with the expression of TNF-alpha in the lung and small intestines.
研究热暴露与脂多糖（LPS）共同作用对大鼠肺和小肠中肿瘤坏死因子-α（TNF-α）表达的影响。
将雄性无特定病原体Wistar大鼠随机分为生理盐水注射常温对照组（C）、生理盐水热暴露组（H）、LPS常温对照组（L）和LPS加 热暴露组（HL）。H组和HL组大鼠置于环境干球温度（Tdb）为35.0±0.5摄氏度的舱室中暴露，C组和L组大鼠置于26±0.5摄氏度环境中暴露。L组和HL组大鼠经尾静脉注射10 mg/kg LPS诱导内毒素血症，C组和H组大鼠注射10 ml/kg。采用ELISA法在不同时间点检测血浆中sTNFrI和sTNFrII水平。采用免疫组化SABC法检测肺和小肠中TNF-α的表达，并在处理后120分钟对肺和小肠损伤进行组织学评估。
热暴露与LPS共同作用导致血浆和组织中TNF-α及其受体sTNFrI和sTNFrII表达显著增强，肺和小肠出现明显的组织病理学损伤。
热暴露与LPS诱导的毒性共同应激与肺和小肠中TNF-α的表达有关。
