CAJ | 학술논문

目的评价内毒素性休克大鼠脑组织和血浆神经球蛋白(Ngb)水平的变化.方法健康清洁级SD大鼠70只,7周龄,雌雄不拘,体重250～300 g,随机分为2组:对照组(C组,n=10)和内毒素性休克组(ES组,n=60).ES组经尾静脉注射内毒素16 ms/ks制备内毒素性休克模型,C组注射等容量生理盐水.ES组于注射内毒素后3、6、12、24、48和72 h(T1-6)时取颈静脉血和脑脊液(CSF)标本,随后处死大鼠,取额叶皮质和海马组织,采用ELISA法和Western blot法测定血浆、CSF、额叶皮质和海马组织Ngb的表达水平,并计算脑水含量.结果与C组比较,ES组T2-6时血浆、CSF、海马和额叶皮质Ngh水平和脑水含量升高(P<0.01);与T2时比较,ES组T3-6时Ngb水平和脑水含量升高(P<0.01);与T5时比较,ES组T2-4时Ngb水平和脑水含量降低(P<0.01),T6时差异无统计学意义(P>0.05);脑水含量与血浆、CSF、海马和额叶皮质Ngb水平呈正相关(r分别为0.631、0.719、0.707和0.706,P<0.01).结论大鼠内毒素性休克时机体Ngh水平上调,此变化可能是机体内源性保护机制之一.
목적 평개내독소성휴극대서뇌조직화혈장신경구단백(Ngb)수평적변화.방법 건강청길급SD대서70지,7주령,자웅불구,체중250～300 g,수궤분위2조:대조조(C조,n=10)화내독소성휴극조(ES조,n=60).ES조경미정맥주사내독소16 ms/ks제비내독소성휴극모형,C조주사등용량생리염수.ES조우주사내독소후3、6、12、24、48화72 h(T1-6)시취경정맥혈화뇌척액(CSF)표본,수후처사대서,취액협피질화해마조직,채용ELISA법화Western blot법측정혈장、CSF、액협피질화해마조직Ngb적표체수평,병계산뇌수함량.결과 여C조비교,ES조T2-6시혈장、CSF、해마화액협피질Ngh수평화뇌수함량승고(P<0.01);여T2시비교,ES조T3-6시Ngb수평화뇌수함량승고(P<0.01);여T5시비교,ES조T2-4시Ngb수평화뇌수함량강저(P<0.01),T6시차이무통계학의의(P>0.05);뇌수함량여혈장、CSF、해마화액협피질Ngb수평정정상관(r분별위0.631、0.719、0.707화0.706,P<0.01).결론 대서내독소성휴극시궤체Ngh수평상조,차변화가능시궤체내원성보호궤제지일.
Objective To investigate the changes in the expression of neuroglobin (Ngb) in the frontal lobe cortex, hippocampus, cerebro-spinal fluid (CSF) and plasma in a rat model of endotoxie shock. Methods Seventy SD rats of both sexes aged 7 weeks weighing 250-300 g were randomly divided into control group (group C, n = 10) and endotoxic shock group (group ES, n =60). LPS 16 mg/kg was injected via the vein in the tail in group ES. In group C, equal volume of normal saline was administered iv instead of LPS. Blood and CSF samples were taken and frontal lobe cortex and hippocampua were removed at 3, 6, 12, 24, 48, and 72 h after LPS administration for determination of Ngb expression by ELISA and Western blotting. Cerebral water content was measured --brain water content = (wet weight- dry weight) ÷ wet weight x 100%.Results The brain water content was significantly increased after LPS administration and peaked at 48 h after LPS. The expression of Ngh was significantly higher in group ES than in group C and peaked at 48 h after LPS (P < 0.01). Conclusion The up-regulation of Ngb induced by endotoxic shock is time-dependent and is one of the endogenous neuron-protective mechanisms of endotoxie shock.