中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2010年
6期
751-753
,共3页
蛋白质加工,转译后%HSP70热休克蛋白质类%心肌%谷氨酰胺%休克,脓毒性
蛋白質加工,轉譯後%HSP70熱休剋蛋白質類%心肌%穀氨酰胺%休剋,膿毒性
단백질가공,전역후%HSP70열휴극단백질류%심기%곡안선알%휴극,농독성
Protein processing,post-translational%HSP70 heat-shock proteins%Myocardium%Glutamine%Shock,septic
目的 探讨O位-N-乙酰葡糖胺(O-GlcNAc)修饰在谷氨酰胺诱导内毒素休克大鼠心肌组织热休克蛋白70(HSP70)表达中的作用.方法 健康雄性SD大鼠32只,随机分为4组(n=8),正常对照组(C组)仅静脉输注乳酸钠林格氏液;LPS组、G+LPS组和A+G+LPS组均静脉注射LPS10 mg/kg,G+LPS组给予LPS前1 h静脉注射谷氨酰胺0.75 g/kg,A+G+LPS组给予LPS前1h依次静脉注射谷氨酰胺0.75 g/kg和O-位-N-乙酰葡萄糖胺糖基转移酶抑制剂四氧嘧啶50 mg/kg.注射LPS后6 h处死大鼠,取心肌组织,测定O-GlcNAc和HSP70的表达水平.结果 与C比较,其他各组心肌O-GlcNAc和HSP70的表达水平均上调(P＜0.05);与LPS组比较,G+LPS组心肌O-GlcNAc和HSP70的表达水平上调(P＜0.05);与G+LPS组比较,A+G+LPS组心肌O-GlcNAc和HSP70的表达水平下调(P＜0.05).结论 O-GlcNAc修饰参与了谷氨酰胺诱导内毒素休克大鼠心肌HSP70表达上调.
目的 探討O位-N-乙酰葡糖胺(O-GlcNAc)脩飾在穀氨酰胺誘導內毒素休剋大鼠心肌組織熱休剋蛋白70(HSP70)錶達中的作用.方法 健康雄性SD大鼠32隻,隨機分為4組(n=8),正常對照組(C組)僅靜脈輸註乳痠鈉林格氏液;LPS組、G+LPS組和A+G+LPS組均靜脈註射LPS10 mg/kg,G+LPS組給予LPS前1 h靜脈註射穀氨酰胺0.75 g/kg,A+G+LPS組給予LPS前1h依次靜脈註射穀氨酰胺0.75 g/kg和O-位-N-乙酰葡萄糖胺糖基轉移酶抑製劑四氧嘧啶50 mg/kg.註射LPS後6 h處死大鼠,取心肌組織,測定O-GlcNAc和HSP70的錶達水平.結果 與C比較,其他各組心肌O-GlcNAc和HSP70的錶達水平均上調(P＜0.05);與LPS組比較,G+LPS組心肌O-GlcNAc和HSP70的錶達水平上調(P＜0.05);與G+LPS組比較,A+G+LPS組心肌O-GlcNAc和HSP70的錶達水平下調(P＜0.05).結論 O-GlcNAc脩飾參與瞭穀氨酰胺誘導內毒素休剋大鼠心肌HSP70錶達上調.
목적 탐토O위-N-을선포당알(O-GlcNAc)수식재곡안선알유도내독소휴극대서심기조직열휴극단백70(HSP70)표체중적작용.방법 건강웅성SD대서32지,수궤분위4조(n=8),정상대조조(C조)부정맥수주유산납림격씨액;LPS조、G+LPS조화A+G+LPS조균정맥주사LPS10 mg/kg,G+LPS조급여LPS전1 h정맥주사곡안선알0.75 g/kg,A+G+LPS조급여LPS전1h의차정맥주사곡안선알0.75 g/kg화O-위-N-을선포도당알당기전이매억제제사양밀정50 mg/kg.주사LPS후6 h처사대서,취심기조직,측정O-GlcNAc화HSP70적표체수평.결과 여C비교,기타각조심기O-GlcNAc화HSP70적표체수평균상조(P＜0.05);여LPS조비교,G+LPS조심기O-GlcNAc화HSP70적표체수평상조(P＜0.05);여G+LPS조비교,A+G+LPS조심기O-GlcNAc화HSP70적표체수평하조(P＜0.05).결론 O-GlcNAc수식삼여료곡안선알유도내독소휴극대서심기HSP70표체상조.
Objective To investigate the role of O-linked N-acetylglutamine (O-GlcNAc) modification in glutamine-induced myocardial heat shock protein (HSP70) expression in a rat model of endotoxic shock. Methods Thirty-two 8 weeks old male SD rats weighing 250-300 g were randomly divided into 4 groups (n = 8 each):group Ⅰ control (group C); group Ⅱ LPS; group Ⅲ G+ LPS and group glutamine + LPS (group A + G + LPS). Endotoxic shock was induced by iv administration of LPS 10 mg/kg in group Ⅱ , Ⅲ and Ⅳ.Glutamine 0.75 g/kg was administered iv at 1 h before iv LPS in group Ⅲ and Ⅳ . Alloxan (an inhibitor ofO-linked N-acetylglucosamine transferase) 50 mg/kg was administered iv together with glutamine at 1 h before LPS in group Ⅳ. The animals were sacrificed at 6 h after iv LPS administration. Their hearts were removed for determination of the expression of O-GlcNAc and HSP70 in myocardium. Results Intravenous LPS significantly up-regulated the expression of O-GlcNAc and HSP70. Glutamine pretreatment further increased the expression of O-GlcNAc and HSP70. The glutamine pretreatment induced increase in O-GlcNAc and HSP70 expression was abolished by concomitant administration of alloxan. Conclusion O-GlcNAc modification may be involved in glutamine-induced myocardial HSP70 expression in endotoxic shock.
