中华医学杂志
中華醫學雜誌
중화의학잡지
National Medical Journal of China
2008年
23期
1648-1650
,共3页
陈晓光%白涛%吴滨阳%王俊科
陳曉光%白濤%吳濱暘%王俊科
진효광%백도%오빈양%왕준과
谷氨酰胺%肿瘤坏死因子%脂多糖类%NF-κB%急性肺损伤
穀氨酰胺%腫瘤壞死因子%脂多糖類%NF-κB%急性肺損傷
곡안선알%종류배사인자%지다당류%NF-κB%급성폐손상
Glutamine%Tumor necrosis factor%Lipopolysaccharides%NF-kappa B%Acute lung injury
目的 探讨谷氨酰胺对脂多糖致急性肺损伤大鼠肺组织核因子(NF)-κB和肺组织病理学变化的影响.方法 静脉注射脂多糖(LPS)5mg/kg复制大鼠急性肺损伤模型.雄性SD大鼠50只,随机分为5组(n=10):对照组(A组);LPS组(B组);C、D、E组为谷氨酰胺+LPS组,分别于LPS注入前1 h、LPS注入同时、LPS注入后1h,静脉注射谷氨酰胺0.75g/kg.于注射LPS后4 h处死动物,测定肺组织NF-κB mRNA表达、肿瘤坏死因子-α(TNF-α)含量、超氧化物歧化酶(SOD)活性以及丙二醛(MDA)含量,HE染色光镜观察肺组织病理变化.结果 与B组比较,C、D组不同程度逆转肺组织SOD活性的下降,抑制肺组织NF-κB mRNA、TNF-α及MDA水平的升高(P＜0.01),光镜下可见肺组织损伤明显减轻.E组上述指标改善不明显.结论 谷氨酰胺早期给药对脂多糖性急性肺损伤起保护效应,其机制与抑制肺组织NF-κB mRNA的过度表达,从而抑制肺部炎症反应有关.
目的 探討穀氨酰胺對脂多糖緻急性肺損傷大鼠肺組織覈因子(NF)-κB和肺組織病理學變化的影響.方法 靜脈註射脂多糖(LPS)5mg/kg複製大鼠急性肺損傷模型.雄性SD大鼠50隻,隨機分為5組(n=10):對照組(A組);LPS組(B組);C、D、E組為穀氨酰胺+LPS組,分彆于LPS註入前1 h、LPS註入同時、LPS註入後1h,靜脈註射穀氨酰胺0.75g/kg.于註射LPS後4 h處死動物,測定肺組織NF-κB mRNA錶達、腫瘤壞死因子-α(TNF-α)含量、超氧化物歧化酶(SOD)活性以及丙二醛(MDA)含量,HE染色光鏡觀察肺組織病理變化.結果 與B組比較,C、D組不同程度逆轉肺組織SOD活性的下降,抑製肺組織NF-κB mRNA、TNF-α及MDA水平的升高(P＜0.01),光鏡下可見肺組織損傷明顯減輕.E組上述指標改善不明顯.結論 穀氨酰胺早期給藥對脂多糖性急性肺損傷起保護效應,其機製與抑製肺組織NF-κB mRNA的過度錶達,從而抑製肺部炎癥反應有關.
목적 탐토곡안선알대지다당치급성폐손상대서폐조직핵인자(NF)-κB화폐조직병이학변화적영향.방법 정맥주사지다당(LPS)5mg/kg복제대서급성폐손상모형.웅성SD대서50지,수궤분위5조(n=10):대조조(A조);LPS조(B조);C、D、E조위곡안선알+LPS조,분별우LPS주입전1 h、LPS주입동시、LPS주입후1h,정맥주사곡안선알0.75g/kg.우주사LPS후4 h처사동물,측정폐조직NF-κB mRNA표체、종류배사인자-α(TNF-α)함량、초양화물기화매(SOD)활성이급병이철(MDA)함량,HE염색광경관찰폐조직병리변화.결과 여B조비교,C、D조불동정도역전폐조직SOD활성적하강,억제폐조직NF-κB mRNA、TNF-α급MDA수평적승고(P＜0.01),광경하가견폐조직손상명현감경.E조상술지표개선불명현.결론 곡안선알조기급약대지다당성급성폐손상기보호효응,기궤제여억제폐조직NF-κB mRNA적과도표체,종이억제폐부염증반응유관.
Objective To investigate the effects of glutamine on the changes of nuclear factor (NF) -KB and lung pathology in acute lung injury. Methods Forty SD rats underwent injection of lipopolysaccharide (LPS) 5 mg/kg into the femoral vein, and were randomly divided into 4 equal groups; Group B; undergoing injection of glutamine 0. 75 g/kg into the femoral vein Ih before LPS injection, Group C undergoing injection of glutamine and LPS simultaneously, and Group D undergoing injection of glutamine Ih after LPS injection, and Group E without glutamine injection. Another 10 rats underwent injection of normal saline to be used as controls (Group A). Four hours after the LPS injection the rats were killed with their lungs taken out. RT-PCR was used to detect the level of nuclear factor (NF)-KB mRNA expression. ELISA was used to detect the tumor necrosis factor (TNF) - in lung. The activity of superoxide dismutase (SOD) was examined by hydroxylamine method, and the malondialdehyde level was determined by thiobarbituric acid (TBA) method. Results The lung NF-KB mRNA expression levels and TNF- levels of Groups B, C, D, and E were all significantly higher than that of Group A ( all P < 0. 01). The lung NF-KB mRNA expression levels and TNF- levels of Groups C and D were all significantly lower than those of Group B (P <0. 01). However, there were no significant differences in lung NF-icB mRNA expression level and TNF- level between Group B and Group E (both P >0. 05). The SOD activity of Group B was significantly lower than that of Group A and the MDA content of Group B was significantly higher than that of Group A ( both P < 0. 05 ). The SOD activity levels of Groups C and D were significantly higher than that of Group B and the MDA content of Groups C and D were significantly lower than that of Group B ( P < 0. 01 or P < 0. 05). However there were no significant differences in lung SDD activity and MDA content between Groups B and E (both P > 0. 05 ). Obvious inflammatory changes were seen in the lungs of Groups B and E at the similar extent. Only slight infiltration could be seen in Groups C and D. The lung of Group A was normal. Conclusion Early glutamine administration protects the lung against acute LPS injury. The mechanism may be inhibition of the overexpression of NF-KB mRNA.
