中国康复
中國康複
중국강복
CHINESE JOURNAL OF REHABILITATION
2015年
1期
10-13
,共4页
孙瑞佼%郭大志%李航%李铭鑫%胡慧军%潘晓雯
孫瑞佼%郭大誌%李航%李銘鑫%鬍慧軍%潘曉雯
손서교%곽대지%리항%리명흠%호혜군%반효문
急性一氧化碳中毒%脱髓鞘%髓鞘碱性蛋白%硫酸软骨素蛋白多糖 NG2%少突胶质前体细胞
急性一氧化碳中毒%脫髓鞘%髓鞘堿性蛋白%硫痠軟骨素蛋白多糖 NG2%少突膠質前體細胞
급성일양화탄중독%탈수초%수초감성단백%류산연골소단백다당 NG2%소돌효질전체세포
acute carbon monoxide poisoning%demyelination%myelin basic protein%chondroitin sulfate proteogly-can NG2%oligodendrocyte precursor cells
目的:通过制备急性一氧化碳中毒(acute carbon monoxide poisoning ,ACOP)大鼠模型,观察大鼠中毒后中枢神经系统髓鞘改变,以及髓鞘标志物髓鞘碱性蛋白(myelin basic protein ,MBP)和少突胶质前体细胞(oligoden‐drocyte precursor cells ,OPCs)特异性细胞标志物硫酸软骨素蛋白多糖 NG2在中毒后表达的变化,为研究 ACOP后中枢神经系统髓鞘脱失的机制提供实验依据。方法:24只雄性健康SD大鼠,随机分为对照组和染毒组各12只。染毒组利用分次腹腔注射CO制作急性中毒模型,对照组注射空气。于造模后1d、3d取材,采用免疫组织化学染色和Western Blot方法检测中毒后中枢神经系统髓鞘的损伤和MBP、NG2表达的变化。结果:免疫组织化学染色结果显示,与对照组比较,染毒组染毒1d后MBP、NG2表达即减少,3d时进一步降低(P<0.05);Western Blot结果显示,染毒组染毒1d后MBP、NG2表达即减少,3d时进一步降低(P<0.05)。结论:ACOP后大鼠发生中枢神经系统脱髓鞘以及OPCs损伤。
目的:通過製備急性一氧化碳中毒(acute carbon monoxide poisoning ,ACOP)大鼠模型,觀察大鼠中毒後中樞神經繫統髓鞘改變,以及髓鞘標誌物髓鞘堿性蛋白(myelin basic protein ,MBP)和少突膠質前體細胞(oligoden‐drocyte precursor cells ,OPCs)特異性細胞標誌物硫痠軟骨素蛋白多糖 NG2在中毒後錶達的變化,為研究 ACOP後中樞神經繫統髓鞘脫失的機製提供實驗依據。方法:24隻雄性健康SD大鼠,隨機分為對照組和染毒組各12隻。染毒組利用分次腹腔註射CO製作急性中毒模型,對照組註射空氣。于造模後1d、3d取材,採用免疫組織化學染色和Western Blot方法檢測中毒後中樞神經繫統髓鞘的損傷和MBP、NG2錶達的變化。結果:免疫組織化學染色結果顯示,與對照組比較,染毒組染毒1d後MBP、NG2錶達即減少,3d時進一步降低(P<0.05);Western Blot結果顯示,染毒組染毒1d後MBP、NG2錶達即減少,3d時進一步降低(P<0.05)。結論:ACOP後大鼠髮生中樞神經繫統脫髓鞘以及OPCs損傷。
목적:통과제비급성일양화탄중독(acute carbon monoxide poisoning ,ACOP)대서모형,관찰대서중독후중추신경계통수초개변,이급수초표지물수초감성단백(myelin basic protein ,MBP)화소돌효질전체세포(oligoden‐drocyte precursor cells ,OPCs)특이성세포표지물류산연골소단백다당 NG2재중독후표체적변화,위연구 ACOP후중추신경계통수초탈실적궤제제공실험의거。방법:24지웅성건강SD대서,수궤분위대조조화염독조각12지。염독조이용분차복강주사CO제작급성중독모형,대조조주사공기。우조모후1d、3d취재,채용면역조직화학염색화Western Blot방법검측중독후중추신경계통수초적손상화MBP、NG2표체적변화。결과:면역조직화학염색결과현시,여대조조비교,염독조염독1d후MBP、NG2표체즉감소,3d시진일보강저(P<0.05);Western Blot결과현시,염독조염독1d후MBP、NG2표체즉감소,3d시진일보강저(P<0.05)。결론:ACOP후대서발생중추신경계통탈수초이급OPCs손상。
Objective:To observe the changes in myelin and expression of myelin basic protein (MBP) and NG2 in the brain tissue of rats through the establishment of the acute carbon monoxide poisoning (ACOP) model ,and to provide experimental evidence for the mechanism of demyelination of the central nervous system after ACOP .Meth‐ods:Twenty‐four male rats were divided into the control group (n=12) and the intoxication group (n=12) random‐ly .Animals in the intoxication group were intraperitoneally injected with pure CO repeatedly ,and those in the con‐trol group with air by the same protocol .The brain tissues were taken from the animals of the two groups at 1st and 3rd day after the establishment of the model .Changes in myelin were observed by immunohistochemical staining , and the expression of MBP and NG2 was detected using immunohistochemistry and Western blot .Results:Immuno‐histochemistry demonstrated that the expression levels of MBP and NG 2 began to decrease at 1st day after ACOP , and there was statistically significant difference in the integral optical density (IOD) level of MBP and NG2 as com‐pared with the control group at 3rd day after ACOP (P<0 .05) .Results of Western blot showed that as compared with the control group ,the expression levels of MBP and NG2 were decreased at 1st day after ACOP ,and decreased further at 3rd day (P<0 .05) .Conclusion:Demyelination and damage of oligodendrocyte precursor cells occurred in the brain tissue of rats after ACOP .