中国组织工程研究
中國組織工程研究
중국조직공정연구
Journal of Clinical Rehabilitative Tissue Engineering Research
2014年
18期
2836-2840
,共5页
实验动物%组织构建%一氧化碳%血红素加氧酶%小鼠%脑病%中毒
實驗動物%組織構建%一氧化碳%血紅素加氧酶%小鼠%腦病%中毒
실험동물%조직구건%일양화탄%혈홍소가양매%소서%뇌병%중독
carbon monoxide poisoning%brain diseases%heme oxygenase-1%mice
背景：研究表明一氧化碳中毒迟发性脑病症状的出现与一氧化碳中毒后神经组织细胞凋亡持续发生关系较大。有关血红素加氧酶的细胞保护作用尤其在脑损伤中的细胞保护作用还存在争议。<br> 目的：观察一氧化碳中毒后不同时间点小鼠脑内血红素加氧酶1 mRNA和蛋白的表达变化。<br> 方法：雄性昆明小鼠随机分为2组，一氧化碳中毒组腹腔注射一氧化碳制备一氧化碳中毒迟发性脑病模型，空气对照组腹腔注射空气。应用原位杂交及 Western blot 法观察两组在不同时间点海马区血红素加氧酶1 mRNA及蛋白表达变化。<br> 结果与结论：空气对照组血红素加氧酶1 mRNA表达阳性细胞较少，染色较浅；一氧化碳中毒组海马阳性细胞数较多，染色较深。血红素加氧酶1 mRNA在1 d表达增加(P<0.01)，3 d达高峰(P<0.01)，5 d时下降(P<0.01)，21 d时仍高于空气对照组(P<0.01)。血红素加氧酶1蛋白表达与血红素加氧酶1 mRNA表达变化相一致。结果表明血红素加氧酶1 mRNA及其蛋白的表达增加可能在一氧化碳中毒所致迟发性脑病的发病机制中起重要作用。
揹景：研究錶明一氧化碳中毒遲髮性腦病癥狀的齣現與一氧化碳中毒後神經組織細胞凋亡持續髮生關繫較大。有關血紅素加氧酶的細胞保護作用尤其在腦損傷中的細胞保護作用還存在爭議。<br> 目的：觀察一氧化碳中毒後不同時間點小鼠腦內血紅素加氧酶1 mRNA和蛋白的錶達變化。<br> 方法：雄性昆明小鼠隨機分為2組，一氧化碳中毒組腹腔註射一氧化碳製備一氧化碳中毒遲髮性腦病模型，空氣對照組腹腔註射空氣。應用原位雜交及 Western blot 法觀察兩組在不同時間點海馬區血紅素加氧酶1 mRNA及蛋白錶達變化。<br> 結果與結論：空氣對照組血紅素加氧酶1 mRNA錶達暘性細胞較少，染色較淺；一氧化碳中毒組海馬暘性細胞數較多，染色較深。血紅素加氧酶1 mRNA在1 d錶達增加(P<0.01)，3 d達高峰(P<0.01)，5 d時下降(P<0.01)，21 d時仍高于空氣對照組(P<0.01)。血紅素加氧酶1蛋白錶達與血紅素加氧酶1 mRNA錶達變化相一緻。結果錶明血紅素加氧酶1 mRNA及其蛋白的錶達增加可能在一氧化碳中毒所緻遲髮性腦病的髮病機製中起重要作用。
배경：연구표명일양화탄중독지발성뇌병증상적출현여일양화탄중독후신경조직세포조망지속발생관계교대。유관혈홍소가양매적세포보호작용우기재뇌손상중적세포보호작용환존재쟁의。<br> 목적：관찰일양화탄중독후불동시간점소서뇌내혈홍소가양매1 mRNA화단백적표체변화。<br> 방법：웅성곤명소서수궤분위2조，일양화탄중독조복강주사일양화탄제비일양화탄중독지발성뇌병모형，공기대조조복강주사공기。응용원위잡교급 Western blot 법관찰량조재불동시간점해마구혈홍소가양매1 mRNA급단백표체변화。<br> 결과여결론：공기대조조혈홍소가양매1 mRNA표체양성세포교소，염색교천；일양화탄중독조해마양성세포수교다，염색교심。혈홍소가양매1 mRNA재1 d표체증가(P<0.01)，3 d체고봉(P<0.01)，5 d시하강(P<0.01)，21 d시잉고우공기대조조(P<0.01)。혈홍소가양매1단백표체여혈홍소가양매1 mRNA표체변화상일치。결과표명혈홍소가양매1 mRNA급기단백적표체증가가능재일양화탄중독소치지발성뇌병적발병궤제중기중요작용。
BACKGROUND:Currently delayed encephalopathy is closely related with the cel apoptosis in nerve tissue after carbon monoxide (CO) poisoning. The protective effect of heme oxygenase-1, especial y in the brain injury remains controversial. <br> OBJECTIVE:To observe heme oxygenase-1 mRNA and protein expression at different time points after CO poisoning in the mouse brain. <br> METHODS:Male Kunming mice, weighing 18-22 g, were randomly divided into CO poisoning group and air control group. The model of delayed encephalopathy after acute CO poisoning was established with intraperitoneal injection of CO. Air control group was intraperitoneal y injected with air. In situ hybridization and western blot analysis were applied to observe the heme oxygenase-1 mRNA and protein expression in the hippocampus of mice in the two groups at different time points. <br> RESULTS AND CONCLUSION:There were few positive cel s for heme oxygenase-1 mRNA expression in the air control group, with light staining;but a large number of positive cel s for heme oxygenase-1 mRNA expression in CO poisoning group, with deep staining. The heme oxygenase-1 mRNA expression was increased at 1 days (P<0.01), reached a peak at 3 days (P<0.01), decreased at 5 days (P<0.01), and stil higher than air control group at 21 days (P<0.01). Changes of heme oxygenase-1 protein expression were consistent with heme oxygenase-1 mRNA expression. The upregulated expression of heme oxygenase-1 mRNA and protein plays a crucial role in the pathogenesis of delayed encephalopathy after CO poisoning.
