摘要
目的探讨高温与脂多糖(LPS)复合应激大鼠肺及小肠组织TNF-α的表达特点。方法雄性SPF级Wistar大鼠随机分为常温+生理盐水组(C组)、高温+生理盐水组(H组)、常温+LPS组(L组)、高温+LPS组(HL组)。置动物于模拟气候舱,HL组、H组暴露环境干球温度(Tdb)为(35.0±0.5)℃,L组和C组Tdb为(26±0.5)℃;HL组和L组动物经尾静脉ivLPS10mg/kg,H组和C组动物经尾静脉iv9g/L NaCl10ml/kg。于各时相点采血ELISA法检测血浆sTNFrⅠ、sTNFrⅡ含量,并于应激120min时,免疫组织化学SABC染色法检测动物肺及小肠组织TNF-α的表达特点,并做常规病理学检查。结果高温与LPS复合应激组动物血浆sTNFrⅠ、sTNFrⅡ含量显著升高,肺及小肠组织TNF-α及其受体sTNFrⅠ和sTNFrⅡ的表达显著增强,组织损伤程度加重。结论高温与LPS复合应激造成的肺及小肠毒性与TNF-α表达密切相关。
Objective To investigate the effects of co-exposure to hyperthermia and lipopolysaccharides（LPS） on tumor necrosis factor-α（TNF-α） expression in the lungs and small intestines of rats.Methods 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 ℃,and those in C and L groups to 26±0.5 ℃.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-α 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.Results Co-exposure to hyperthermia and LPS caused significantly enhanced expressions of TNF-α and its receptor sTNFrI and sTNFrⅡ in the plasma and tissues and obvious histopathological damage in the lung and small intestines.Conclusion Co-stress of hyperthermia and LPS-induced toxicity is associated with the expression of TNF-α in the lung and small intestines.
出处
《南方医科大学学报》
CAS
CSCD
北大核心
2010年第2期263-265,269,共4页
Journal of Southern Medical University
基金
中国人民解放军广州军区总医院刘坚院长基金
广东省科技计划项目
关键词
过热
脂多糖
全身炎症反应综合征
免疫组化
肿瘤坏死因子-Α
hyperthermia
lipopolysaccharides
systemic inflammatory response syndrome
immunohistochemistry
tumor necrosis factor-α
