中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2008年
9期
832-835
,共4页
胆碱能拮抗剂%内毒素血症%脑损伤%NF-κB%一氧化氮合酶
膽堿能拮抗劑%內毒素血癥%腦損傷%NF-κB%一氧化氮閤酶
담감능길항제%내독소혈증%뇌손상%NF-κB%일양화담합매
Cholinergic antagonists%Endotoxemia%Brain injuries%NF-kappa B%Nitric-oxide syhthase
目的 评价戊乙奎醚预先给药对大鼠内毒素性脑损伤时NF-κB和诱导型一氧化氮合酶(iNOS)表达的影响.方法 雄性SD大鼠105只,体重200～220 g,随机分为5组(n=21),D1组、D2组或D3组分别腹腔注射戊乙奎醚0.05、0.15、0.45 mg/kg,NS组和L组给予等容量生理盐水,10min后L组、D1组、D2组和D3组经左颈内动脉注射脂多糖150 μg,NS组给予等容量生理盐水.分别于注射戊乙奎醚后4、6和12 h处死7只大鼠,取脑组织,测定脑组织含水量、NF-κB和iNOS表达水平,光镜和电镜下观察脑组织病理学结果.结果 与NS组相比,L组、D1组、D2组和D3组脑组织含水量、NF-κB和iNOS表达增加(P<0.05);与L组相比,D1组脑组织含水量、NF-κB和iNOS表达差异无统计学意义(P0.05),D2组和D3组脑组织含水量、NF-κB和iNOS表达降低(P<0.05).D2组和D3组脑组织病理学损伤轻于L组.结论 戊乙奎醚0.15、0.45 mg/kg预先给药减轻大鼠内毒素性脑损伤的机制与抑制脑组织NF-κB和iNOS表达上调有关.
目的 評價戊乙奎醚預先給藥對大鼠內毒素性腦損傷時NF-κB和誘導型一氧化氮閤酶(iNOS)錶達的影響.方法 雄性SD大鼠105隻,體重200～220 g,隨機分為5組(n=21),D1組、D2組或D3組分彆腹腔註射戊乙奎醚0.05、0.15、0.45 mg/kg,NS組和L組給予等容量生理鹽水,10min後L組、D1組、D2組和D3組經左頸內動脈註射脂多糖150 μg,NS組給予等容量生理鹽水.分彆于註射戊乙奎醚後4、6和12 h處死7隻大鼠,取腦組織,測定腦組織含水量、NF-κB和iNOS錶達水平,光鏡和電鏡下觀察腦組織病理學結果.結果 與NS組相比,L組、D1組、D2組和D3組腦組織含水量、NF-κB和iNOS錶達增加(P<0.05);與L組相比,D1組腦組織含水量、NF-κB和iNOS錶達差異無統計學意義(P0.05),D2組和D3組腦組織含水量、NF-κB和iNOS錶達降低(P<0.05).D2組和D3組腦組織病理學損傷輕于L組.結論 戊乙奎醚0.15、0.45 mg/kg預先給藥減輕大鼠內毒素性腦損傷的機製與抑製腦組織NF-κB和iNOS錶達上調有關.
목적 평개무을규미예선급약대대서내독소성뇌손상시NF-κB화유도형일양화담합매(iNOS)표체적영향.방법 웅성SD대서105지,체중200～220 g,수궤분위5조(n=21),D1조、D2조혹D3조분별복강주사무을규미0.05、0.15、0.45 mg/kg,NS조화L조급여등용량생리염수,10min후L조、D1조、D2조화D3조경좌경내동맥주사지다당150 μg,NS조급여등용량생리염수.분별우주사무을규미후4、6화12 h처사7지대서,취뇌조직,측정뇌조직함수량、NF-κB화iNOS표체수평,광경화전경하관찰뇌조직병이학결과.결과 여NS조상비,L조、D1조、D2조화D3조뇌조직함수량、NF-κB화iNOS표체증가(P<0.05);여L조상비,D1조뇌조직함수량、NF-κB화iNOS표체차이무통계학의의(P0.05),D2조화D3조뇌조직함수량、NF-κB화iNOS표체강저(P<0.05).D2조화D3조뇌조직병이학손상경우L조.결론 무을규미0.15、0.45 mg/kg예선급약감경대서내독소성뇌손상적궤제여억제뇌조직NF-κB화iNOS표체상조유관.
Objective To investigate the effects of penehyclidine hydrochloride (PHCD) pretreatment on expression of NF-κB and iNOS in rats with LPS-induced brain injury. Methods One hundred and five male SD rats weighing 200-220 g were randomly divided into 5 groups (n=21 each): group Ⅰ normal saline (NS);group Ⅱ LPS (L);group Ⅲ,Ⅳ,Ⅴ PHCD 0.05, 0.15, 0.45 mg/kg (D1,2,3). The animals were anesthetized with chloral hydrate 350 mg/kg. Brain injury was induced by intra-arterial LPS 150 μg administered via left internal carotid artery in group Ⅱ-Ⅴ. In group Ⅲ,Ⅳ, and Ⅴ PHCD 0.05, 0.15 and 0.45 mg/kg were given intraperitoneally (IP) at 10 min before intra-arterial LPS. The animals were decapitated at 4, 6 and 12 h after administration of PHCD (n=7 at each time point in each group). The brains were immediately removed for determination of water content, expression of NF-κB and iNOS protein and examination with light and electron microscope. Results Water content of the brain and expression of NF-κB and iNOS protein were significantly higher in group L, D1, D2 and D3 than in group NS and were significantly lower in group D2 and D3 than in group L. Intra-arterial LPS produced severe damage to the brain which was significantly attenuated by PHCD in group D2 and D3. Conclusion PHCD 0.15,0.45 mg/kg pretreatment can attenuate LPS-induced brain injury by inhibiting the up-regulation of expression of NF-κB and iNOS.
