中国危重病急救医学
中國危重病急救醫學
중국위중병급구의학
CHINESE CRITICAL CARE MEDICINE
2009年
7期
387-389,插1
,共4页
余林中%胡孔友%刘建新%刁建新%王丽
餘林中%鬍孔友%劉建新%刁建新%王麗
여림중%호공우%류건신%조건신%왕려
肺损伤,急性%内毒素%信号转导和转录激活因子1
肺損傷,急性%內毒素%信號轉導和轉錄激活因子1
폐손상,급성%내독소%신호전도화전록격활인자1
acute lung injury%endotoxin%signal transducer and activator of transcription 1
目的 探讨信号转导和转录激活因子1(STAT1)在内毒素致急性肺损伤(ALI)大鼠肺组织中的表达及其调控作用.方法 静脉注射内毒素脂多糖(LPS)制备大鼠ALI模型.将动物随机分为对照组、LPS组、地塞米松(DEX)干预组;DEX干预组灌胃DEX 0.135 mg/kg,对照组和LPS组分别灌胃等量生理盐水,连用5 d后LPS组和DEX干预组经尾静脉注射LPS 5 mg/kg,对照组以生理盐水1 ml替代.于致伤后1、2、4、8、16 h各处死6只大鼠,取肺组织,用蛋白质免疫印迹法(Western blotting)测定STAT1表达的动态变化,光镜下观察肺组织病理学改变.结果 与对照组比较,LPS组STAT1的活化从1 h开始增高,4 h达高峰,然后逐渐下降;2、4、8 h时STAT1表达显著升高(P均<0.01);DEX干预组STAT1表达趋势同LPS组,但2、4、8 h时STAT1表达显著低于LPS组(P均<0.05).结论 内毒素致ALI中存在STAT1异常表达;STAT1参与了肺组织炎症的形成.
目的 探討信號轉導和轉錄激活因子1(STAT1)在內毒素緻急性肺損傷(ALI)大鼠肺組織中的錶達及其調控作用.方法 靜脈註射內毒素脂多糖(LPS)製備大鼠ALI模型.將動物隨機分為對照組、LPS組、地塞米鬆(DEX)榦預組;DEX榦預組灌胃DEX 0.135 mg/kg,對照組和LPS組分彆灌胃等量生理鹽水,連用5 d後LPS組和DEX榦預組經尾靜脈註射LPS 5 mg/kg,對照組以生理鹽水1 ml替代.于緻傷後1、2、4、8、16 h各處死6隻大鼠,取肺組織,用蛋白質免疫印跡法(Western blotting)測定STAT1錶達的動態變化,光鏡下觀察肺組織病理學改變.結果 與對照組比較,LPS組STAT1的活化從1 h開始增高,4 h達高峰,然後逐漸下降;2、4、8 h時STAT1錶達顯著升高(P均<0.01);DEX榦預組STAT1錶達趨勢同LPS組,但2、4、8 h時STAT1錶達顯著低于LPS組(P均<0.05).結論 內毒素緻ALI中存在STAT1異常錶達;STAT1參與瞭肺組織炎癥的形成.
목적 탐토신호전도화전록격활인자1(STAT1)재내독소치급성폐손상(ALI)대서폐조직중적표체급기조공작용.방법 정맥주사내독소지다당(LPS)제비대서ALI모형.장동물수궤분위대조조、LPS조、지새미송(DEX)간예조;DEX간예조관위DEX 0.135 mg/kg,대조조화LPS조분별관위등량생리염수,련용5 d후LPS조화DEX간예조경미정맥주사LPS 5 mg/kg,대조조이생리염수1 ml체대.우치상후1、2、4、8、16 h각처사6지대서,취폐조직,용단백질면역인적법(Western blotting)측정STAT1표체적동태변화,광경하관찰폐조직병이학개변.결과 여대조조비교,LPS조STAT1적활화종1 h개시증고,4 h체고봉,연후축점하강;2、4、8 h시STAT1표체현저승고(P균<0.01);DEX간예조STAT1표체추세동LPS조,단2、4、8 h시STAT1표체현저저우LPS조(P균<0.05).결론 내독소치ALI중존재STAT1이상표체;STAT1삼여료폐조직염증적형성.
Objective To investigate the expression and regulatory effect of signal transducer and activator of transcription 1 (STAT1) in acute lung injury (ALI) induced by endotoxin. Methods ALI model was induced by intravenous lipopolysaccharide (LPS). Wistar rats were randomly divided into three groups, the control group, LPS group, dexamethasone (DEX) group. Each group was subdivided into five subgroups according to the time after administration of endotoxin (1, 2, 4, 8 and 16 hours), except the control group. Rats were given normal saline by gavage in control group and LPS group, and 0.135 mg/kg DEX in DEX group for 5 days. Six rats were sacrificed at different time points after normal saline or LPS injection. The lungs were harvested for microscopic examination. Western blotting was used to examine protein expression of STAT1 in lung tissue. Results In LPS group the levels of STAT1 began to increase at 1 hour, reaching the peak value at 4 hours, then declined gradually. There was a significant difference at 2, 4, 8 hours (all P<0.01). The expression trend for STAT1 was similar between DEX and LPS groups, but the levels of STAT1 were significantly decreased in DEX group at 2, 4, 8 hours compared with the LPS group (all P<0.05). Conclusion There is abnormal expression of STAT1 in the lung tissue of ALI. The abnormal STAT1 expression takes part in the inflammatory formation of lung tissue in ALI.