南方医科大学学报
南方醫科大學學報
남방의과대학학보
JOURNAL OF SOUTHERN MEDICAL UNIVERSITY
2010年
2期
263-265,269
,共4页
左丹%周望梅%郭冰冰%梅桂萍
左丹%週望梅%郭冰冰%梅桂萍
좌단%주망매%곽빙빙%매계평
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
過熱%脂多糖%全身炎癥反應綜閤徵%免疫組化%腫瘤壞死因子-α
과열%지다당%전신염증반응종합정%면역조화%종류배사인자-α
hyperthermia%lipopolysaccharides%systemic inflammatory response syndrome%immunohistochemistry%tumor necrosis factor-α
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iv LPS 10 mg/kg,H组和C组动物经尾静脉iv 9g/LNaCl 10 ml/kg.于各时相点采血ELISA法检测血浆sTNFr Ⅰ、sTNFr Ⅱ含量.并于应激120 min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sTNFr Ⅰ、sTNFr Ⅱ含量显著升高,肺及小肠组织TNF-α及其受体sTNFr Ⅰ和sTNFr Ⅱ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.
目的 探討高溫與脂多糖(LPS)複閤應激大鼠肺及小腸組織TNF-α的錶達特點.方法 雄性SPF級Wistar大鼠隨機分為常溫+生理鹽水組(C組)、高溫+生理鹽水組(H組)、常溫+LPS組(L組)、高溫+LPS組(HL組).置動物于模擬氣候艙,HL組、H組暴露環境榦毬溫度(Tdb)為(35.0±0.5)℃.L組和C組Tdb為(26±0.5)℃;HL組和L組動物經尾靜脈iv LPS 10 mg/kg,H組和C組動物經尾靜脈iv 9g/LNaCl 10 ml/kg.于各時相點採血ELISA法檢測血漿sTNFr Ⅰ、sTNFr Ⅱ含量.併于應激120 min時,免疫組織化學SABC染色法檢測動物肺及小腸組織TNF-α的錶達特點,併做常規病理學檢查.結果 高溫與LPS複閤應激組動物血漿sTNFr Ⅰ、sTNFr Ⅱ含量顯著升高,肺及小腸組織TNF-α及其受體sTNFr Ⅰ和sTNFr Ⅱ的錶達顯著增彊,組織損傷程度加重.結論高溫與LPS複閤應激造成的肺及小腸毒性與TNF-α錶達密切相關.
목적 탐토고온여지다당(LPS)복합응격대서폐급소장조직TNF-α적표체특점.방법 웅성SPF급Wistar대서수궤분위상온+생리염수조(C조)、고온+생리염수조(H조)、상온+LPS조(L조)、고온+LPS조(HL조).치동물우모의기후창,HL조、H조폭로배경간구온도(Tdb)위(35.0±0.5)℃.L조화C조Tdb위(26±0.5)℃;HL조화L조동물경미정맥iv LPS 10 mg/kg,H조화C조동물경미정맥iv 9g/LNaCl 10 ml/kg.우각시상점채혈ELISA법검측혈장sTNFr Ⅰ、sTNFr Ⅱ함량.병우응격120 min시,면역조직화학SABC염색법검측동물폐급소장조직TNF-α적표체특점,병주상규병이학검사.결과 고온여LPS복합응격조동물혈장sTNFr Ⅰ、sTNFr Ⅱ함량현저승고,폐급소장조직TNF-α급기수체sTNFr Ⅰ화sTNFr Ⅱ적표체현저증강,조직손상정도가중.결론고온여LPS복합응격조성적폐급소장독성여TNF-α표체밀절상관.
Objective To investigate the effects of co-exposure to hyperthermia and lipoopolysaccharides (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 immanohistocbemical 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.