中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2011年
5期
621-623
,共3页
二异丙酚%脑损伤%内毒素血症
二異丙酚%腦損傷%內毒素血癥
이이병분%뇌손상%내독소혈증
Propofol%Brain injuries%Endotoxemia
目的 评价异丙酚对大鼠内毒索性脑损伤的影响.方法 健康清洁级SD大鼠54只,周龄6周,体重200～250 g,采用随机数字表法,将大鼠随机分为3组:对照组(C组,n=6)、脂多糖(LPS)组(L组,n=24)和异丙酚组(P组,n=24).L组和P组由左颈内动脉注射LPS 1 mg/kg制备内毒素性脑损伤模型,P组注射LPS后即刻腹腔注射异丙酚100 mg/kg,L组腹腔注射等容量生理盐水,C组分别于左颈内动脉和腹腔注射与LPS和异丙酚等容量生理盐水.C组于腹腔给药后24 h时.L组和P组分别于腹腔给药后6、24、48和72 h时随机处死6只大鼠,取脑组织,测定脑含水量、高迁移率族蛋白1(HMGB1)表达和NF-κB活性,光镜下观察脑组织病理学结果.脑含水量与HMGB1表达、NF-κB活性间进行直线相关分析.结果 与C组比较,L组脑含水量升高,HMGB1表达上调,NF-κB活性升高(P＜0.05);与L组比较,P组脑含水量降低,HMGB1表达下调,NF-κB活性降低(P＜0.05);P组脑组织病理学损伤程度轻于L组;脑含水量与HMGB1表达、NF-κB活性呈正相关(r分别为0.692和0.709,P＜0.05).结论 异丙酚可减轻大鼠内毒索性脑损伤,其机制与减轻脑组织炎性反应有关.
目的 評價異丙酚對大鼠內毒索性腦損傷的影響.方法 健康清潔級SD大鼠54隻,週齡6週,體重200～250 g,採用隨機數字錶法,將大鼠隨機分為3組:對照組(C組,n=6)、脂多糖(LPS)組(L組,n=24)和異丙酚組(P組,n=24).L組和P組由左頸內動脈註射LPS 1 mg/kg製備內毒素性腦損傷模型,P組註射LPS後即刻腹腔註射異丙酚100 mg/kg,L組腹腔註射等容量生理鹽水,C組分彆于左頸內動脈和腹腔註射與LPS和異丙酚等容量生理鹽水.C組于腹腔給藥後24 h時.L組和P組分彆于腹腔給藥後6、24、48和72 h時隨機處死6隻大鼠,取腦組織,測定腦含水量、高遷移率族蛋白1(HMGB1)錶達和NF-κB活性,光鏡下觀察腦組織病理學結果.腦含水量與HMGB1錶達、NF-κB活性間進行直線相關分析.結果 與C組比較,L組腦含水量升高,HMGB1錶達上調,NF-κB活性升高(P＜0.05);與L組比較,P組腦含水量降低,HMGB1錶達下調,NF-κB活性降低(P＜0.05);P組腦組織病理學損傷程度輕于L組;腦含水量與HMGB1錶達、NF-κB活性呈正相關(r分彆為0.692和0.709,P＜0.05).結論 異丙酚可減輕大鼠內毒索性腦損傷,其機製與減輕腦組織炎性反應有關.
목적 평개이병분대대서내독색성뇌손상적영향.방법 건강청길급SD대서54지,주령6주,체중200～250 g,채용수궤수자표법,장대서수궤분위3조:대조조(C조,n=6)、지다당(LPS)조(L조,n=24)화이병분조(P조,n=24).L조화P조유좌경내동맥주사LPS 1 mg/kg제비내독소성뇌손상모형,P조주사LPS후즉각복강주사이병분100 mg/kg,L조복강주사등용량생리염수,C조분별우좌경내동맥화복강주사여LPS화이병분등용량생리염수.C조우복강급약후24 h시.L조화P조분별우복강급약후6、24、48화72 h시수궤처사6지대서,취뇌조직,측정뇌함수량、고천이솔족단백1(HMGB1)표체화NF-κB활성,광경하관찰뇌조직병이학결과.뇌함수량여HMGB1표체、NF-κB활성간진행직선상관분석.결과 여C조비교,L조뇌함수량승고,HMGB1표체상조,NF-κB활성승고(P＜0.05);여L조비교,P조뇌함수량강저,HMGB1표체하조,NF-κB활성강저(P＜0.05);P조뇌조직병이학손상정도경우L조;뇌함수량여HMGB1표체、NF-κB활성정정상관(r분별위0.692화0.709,P＜0.05).결론 이병분가감경대서내독색성뇌손상,기궤제여감경뇌조직염성반응유관.
Objective To investigate the effects of propofol on lipopolysaccharide (LPS)-induced brain injury in rats.Methods Fifty-four pathogen-free SD rats of both sexes, aged 6 weeks, weighing 200-250 g, were randomly divided into 3 groups: control group (group C, n = 6) ; LPS group (group L, n = 24) ; propofol group (group P, n = 24) . Brain injury was produced by injection of LPS 1 mg/kg via the left internal carotid artery in L and P groups. Propofol 100 mg/kg was injected intraperitonealry immediately after the LPS administration in group P, while the equal volume of normal saline was given instead of propofol in group L. The equal volume of normal saline was given instead of LPS and propofol in group C. Six rats in each group were sacrificed and the brain tissues were immediately removed at 24 h after intraperitoneal administration in group C, and at 6, 24, 48 and 72 h after intraperitoneal administration in L and P groups for determination of brain water content, high-mobility group box 1 ( HMGB1) expression and NF-κB activity, and microscopic examination. Results The brain water content and NF-kB activity were significantly increased, and HMGB1 expression was up-regulated in group L as compared to group C (P ＜ 0.05) . The brain water content, expression of HMGB1 and NF-kB activity were significantly lower in group P than in group L ( P ＜ 0.05) . The microscopic examination showed that brain injury was attenuated in group P compared with group L. The brain water content was positively correlated with the HMGB1 expression and NF- κB activity (r = 0.692 and 0.769 respectively, P ＜ 0.05). Conclusion Propofol can reduce the LPS- induced brain injury by reducing inflammatory response of the brain tissues.
