中国医药指南
中國醫藥指南
중국의약지남
CHINA MEDICINE GUIDE
2013年
4期
55-57
,共3页
糖尿病%NF-κBp65蛋白%认知功能障碍%体外循环%发病机制
糖尿病%NF-κBp65蛋白%認知功能障礙%體外循環%髮病機製
당뇨병%NF-κBp65단백%인지공능장애%체외순배%발병궤제
Diabetes%NF-κBp65 protein%Cognitive dysfunction%Cardiopulmonary bypass%Pathogenesis
目的?探讨糖尿病大鼠体外循环(cardiopulmonary?bypass,CPB)术后认知功能的变化.方法?将SD大鼠随机分成非糖尿病CPB组(A组)及糖尿病CPB组(B组).腹腔一次性注射1%STZ?(溶于pH?4.2,0.1%mol/L柠檬酸-柠檬酸钠缓冲液)60mg/kg建立糖尿病模型,糖尿病模型建立后第7周建立CPB模型.观察糖尿病大鼠CPB后认知功能的变化以及海马NF-κBp65蛋白的表达,抽取静脉血用ELISA法检测TNF-α及IL-10含量.结果?各组大鼠术前认知功能测试无显著性差异(P>0.05),体外循环后5天各组差异显著,糖尿病CPB组(B组)电击次数明显增加(P<0.05,P<0.01),差别有显著性.B组大鼠脑组织海马NF-κBp65蛋白阳性细胞数明显增多,差异有统计学意义(P<0.01).两组大鼠血清TNF-α及IL-10含量均有增高,B组大鼠增高更加明显,差异有统计学意义(P<0.05).结论?糖尿病可以引发并加重体外循环后大鼠脑内NF-κBp65蛋白过度表达,促使细胞因子释放,对脑组织产生损伤并出现认知功能障碍.糖尿病通过NF-κBp65蛋白途径参与糖尿病体外循环术后认知功能障碍的发生发展.
目的?探討糖尿病大鼠體外循環(cardiopulmonary?bypass,CPB)術後認知功能的變化.方法?將SD大鼠隨機分成非糖尿病CPB組(A組)及糖尿病CPB組(B組).腹腔一次性註射1%STZ?(溶于pH?4.2,0.1%mol/L檸檬痠-檸檬痠鈉緩遲液)60mg/kg建立糖尿病模型,糖尿病模型建立後第7週建立CPB模型.觀察糖尿病大鼠CPB後認知功能的變化以及海馬NF-κBp65蛋白的錶達,抽取靜脈血用ELISA法檢測TNF-α及IL-10含量.結果?各組大鼠術前認知功能測試無顯著性差異(P>0.05),體外循環後5天各組差異顯著,糖尿病CPB組(B組)電擊次數明顯增加(P<0.05,P<0.01),差彆有顯著性.B組大鼠腦組織海馬NF-κBp65蛋白暘性細胞數明顯增多,差異有統計學意義(P<0.01).兩組大鼠血清TNF-α及IL-10含量均有增高,B組大鼠增高更加明顯,差異有統計學意義(P<0.05).結論?糖尿病可以引髮併加重體外循環後大鼠腦內NF-κBp65蛋白過度錶達,促使細胞因子釋放,對腦組織產生損傷併齣現認知功能障礙.糖尿病通過NF-κBp65蛋白途徑參與糖尿病體外循環術後認知功能障礙的髮生髮展.
목적?탐토당뇨병대서체외순배(cardiopulmonary?bypass,CPB)술후인지공능적변화.방법?장SD대서수궤분성비당뇨병CPB조(A조)급당뇨병CPB조(B조).복강일차성주사1%STZ?(용우pH?4.2,0.1%mol/L저몽산-저몽산납완충액)60mg/kg건립당뇨병모형,당뇨병모형건립후제7주건립CPB모형.관찰당뇨병대서CPB후인지공능적변화이급해마NF-κBp65단백적표체,추취정맥혈용ELISA법검측TNF-α급IL-10함량.결과?각조대서술전인지공능측시무현저성차이(P>0.05),체외순배후5천각조차이현저,당뇨병CPB조(B조)전격차수명현증가(P<0.05,P<0.01),차별유현저성.B조대서뇌조직해마NF-κBp65단백양성세포수명현증다,차이유통계학의의(P<0.01).량조대서혈청TNF-α급IL-10함량균유증고,B조대서증고경가명현,차이유통계학의의(P<0.05).결론?당뇨병가이인발병가중체외순배후대서뇌내NF-κBp65단백과도표체,촉사세포인자석방,대뇌조직산생손상병출현인지공능장애.당뇨병통과NF-κBp65단백도경삼여당뇨병체외순배술후인지공능장애적발생발전.
Objective?Diabetic?rats?cardiopulmonary?bypass?(cardiopulmonary?bypass,?CPB)?changes?in?postoperative?cognitive?function..?Methods?SD?rats?were?randomly?divided?into?non-diabetic?CPB?group?(A)?and?diabetes?CPB?group?(B).?Intraperitoneal?single?injection?of?1%?STZ?(dissolved?in?pH?4.2,?0.1%?mol/L?citric?acid?-?sodium?citrate?buffer)?60mg/kg?create?a?model?of?diabetes,?diabetic?model?after?7?weeks?in?CPB?model.?Of?diabetic?rats?after?CPB?cognitive function changes, and the hippocampus the NF-κBp65 protein expression to extract the venous blood ELISA was used to detect TNF-αand IL-10 levels.?Results?Tests of cognitive function in rats preoperative significant difference (P>0.05), five days after cardiopulmonary bypass groups significantly different, diabetes CPB group (B) the number of shocks increased significantly (P<0.05,?P<0.01), the difference is significant. Group B rat brain hippocampus the NF-κBp65 protein-positive cells increased significantly, and the difference was statistically significant (P<0.01). The two groups of serum TNF-αand IL-10 levels have increased more significantly increased B rats, the difference was statistically significant (P<0.05).?Conclusions?Diabetes?can?trigger?and?aggravate cardiopulmonary bypass the rat brain of NF-κBp65 protein overexpression, prompting the release of cytokines, brain tissue damage and cognitive dysfunction. Diabetes through NF-κBp65 protein pathways involved in the development of diabetes the extracorporeal circulation postoperative cognitive dysfunction.
