河北医药
河北醫藥
하북의약
HEBEI MEDICAL JOURNAL
2014年
21期
3220-3222
,共3页
黄敏%张红梅%段微%尹虹祥%许康
黃敏%張紅梅%段微%尹虹祥%許康
황민%장홍매%단미%윤홍상%허강
糖尿病%脑梗死%炎性因子%调控因子%血液流变学
糖尿病%腦梗死%炎性因子%調控因子%血液流變學
당뇨병%뇌경사%염성인자%조공인자%혈액류변학
diabetes mellitus%cerebral infarction%inflammatory cytokines%regulatory factor%hemorheology
目的：探讨2型糖尿病合并脑梗死患者的炎症因子，包括超敏C-反应蛋白（hs-CRP）、白介素6（IL-6）、IL-8、肿瘤坏死因子-α（ TNF-α）水平，和调控因子内源性核因子κB（ NF-κB）活性及血液流变学指标的变化。方法对照组、单纯脑梗死组、单纯2型糖尿病组、2型糖尿病合并脑梗死组，每组60例，共240例。血清hs-CRP采用免疫荧光分析法检测，血清IL-6、IL-8、TNF-α采用ELISA法检测。外周血NF-κB活性采用免疫组织化学法检测。全自动血液流变仪测定血液流变学指标。将2型糖尿病合并脑梗死组的外周血NF-κB活性与血液流变学指标进行相关性分析。结果2型糖尿病合并脑梗死组血清 hs-CRP、IL-6、IL-8、TNF-α水平分别为（14．33±5．65） mg/L，（25．45±6．98）ng/L，（103．35±21．58）ng/L，（35．69±6．72）ng/L，均显著高于其他3组（ P ＜0．01）。2型糖尿病合并脑梗死组外周血NF-κB活性为（133．68±23．02）pg/ml，显著高于其他3组（ P ＜0．01）。2型糖尿病合并脑梗死组全血低切黏度、全血高切黏度、血浆黏度、纤维蛋白原、红细胞聚集指数和血小板最大聚集率非别为（30．51±4．14）mPa· s，（6．99±1．05）mPa· s，（2．12±0．27）mPa · s，（6．75±0．84）g/L，（9．91±1．56）和（87．14±15．72）％，均显著高于其他3组（ P ＜0．01）。2型糖尿病合并脑梗死患者中NF-κB活性与全血低切黏度、高切黏度、血浆黏度、纤维蛋白原、红细胞聚集指数以及血小板最大聚集率呈显著正相关（ r ＝0．637、0．529、0．502、0．644、0．517、0．681， P均＜0．01）。结论在长期高血糖作用下，炎性因子（ hs-CRP、IL-6、IL-8和TNF -α）水平升高，炎性因子可以激活NF-κB，导致血液流变学异常，使血液处于高粘、高凝状态，血流缓慢，易于形成血栓，引起和加速2型糖尿病合并脑梗死的发生和发展；NF-κB可作为2型糖尿病合并脑梗死患者治疗中新型的药物靶点。
目的：探討2型糖尿病閤併腦梗死患者的炎癥因子，包括超敏C-反應蛋白（hs-CRP）、白介素6（IL-6）、IL-8、腫瘤壞死因子-α（ TNF-α）水平，和調控因子內源性覈因子κB（ NF-κB）活性及血液流變學指標的變化。方法對照組、單純腦梗死組、單純2型糖尿病組、2型糖尿病閤併腦梗死組，每組60例，共240例。血清hs-CRP採用免疫熒光分析法檢測，血清IL-6、IL-8、TNF-α採用ELISA法檢測。外週血NF-κB活性採用免疫組織化學法檢測。全自動血液流變儀測定血液流變學指標。將2型糖尿病閤併腦梗死組的外週血NF-κB活性與血液流變學指標進行相關性分析。結果2型糖尿病閤併腦梗死組血清 hs-CRP、IL-6、IL-8、TNF-α水平分彆為（14．33±5．65） mg/L，（25．45±6．98）ng/L，（103．35±21．58）ng/L，（35．69±6．72）ng/L，均顯著高于其他3組（ P ＜0．01）。2型糖尿病閤併腦梗死組外週血NF-κB活性為（133．68±23．02）pg/ml，顯著高于其他3組（ P ＜0．01）。2型糖尿病閤併腦梗死組全血低切黏度、全血高切黏度、血漿黏度、纖維蛋白原、紅細胞聚集指數和血小闆最大聚集率非彆為（30．51±4．14）mPa· s，（6．99±1．05）mPa· s，（2．12±0．27）mPa · s，（6．75±0．84）g/L，（9．91±1．56）和（87．14±15．72）％，均顯著高于其他3組（ P ＜0．01）。2型糖尿病閤併腦梗死患者中NF-κB活性與全血低切黏度、高切黏度、血漿黏度、纖維蛋白原、紅細胞聚集指數以及血小闆最大聚集率呈顯著正相關（ r ＝0．637、0．529、0．502、0．644、0．517、0．681， P均＜0．01）。結論在長期高血糖作用下，炎性因子（ hs-CRP、IL-6、IL-8和TNF -α）水平升高，炎性因子可以激活NF-κB，導緻血液流變學異常，使血液處于高粘、高凝狀態，血流緩慢，易于形成血栓，引起和加速2型糖尿病閤併腦梗死的髮生和髮展；NF-κB可作為2型糖尿病閤併腦梗死患者治療中新型的藥物靶點。
목적：탐토2형당뇨병합병뇌경사환자적염증인자，포괄초민C-반응단백（hs-CRP）、백개소6（IL-6）、IL-8、종류배사인자-α（ TNF-α）수평，화조공인자내원성핵인자κB（ NF-κB）활성급혈액류변학지표적변화。방법대조조、단순뇌경사조、단순2형당뇨병조、2형당뇨병합병뇌경사조，매조60례，공240례。혈청hs-CRP채용면역형광분석법검측，혈청IL-6、IL-8、TNF-α채용ELISA법검측。외주혈NF-κB활성채용면역조직화학법검측。전자동혈액류변의측정혈액류변학지표。장2형당뇨병합병뇌경사조적외주혈NF-κB활성여혈액류변학지표진행상관성분석。결과2형당뇨병합병뇌경사조혈청 hs-CRP、IL-6、IL-8、TNF-α수평분별위（14．33±5．65） mg/L，（25．45±6．98）ng/L，（103．35±21．58）ng/L，（35．69±6．72）ng/L，균현저고우기타3조（ P ＜0．01）。2형당뇨병합병뇌경사조외주혈NF-κB활성위（133．68±23．02）pg/ml，현저고우기타3조（ P ＜0．01）。2형당뇨병합병뇌경사조전혈저절점도、전혈고절점도、혈장점도、섬유단백원、홍세포취집지수화혈소판최대취집솔비별위（30．51±4．14）mPa· s，（6．99±1．05）mPa· s，（2．12±0．27）mPa · s，（6．75±0．84）g/L，（9．91±1．56）화（87．14±15．72）％，균현저고우기타3조（ P ＜0．01）。2형당뇨병합병뇌경사환자중NF-κB활성여전혈저절점도、고절점도、혈장점도、섬유단백원、홍세포취집지수이급혈소판최대취집솔정현저정상관（ r ＝0．637、0．529、0．502、0．644、0．517、0．681， P균＜0．01）。결론재장기고혈당작용하，염성인자（ hs-CRP、IL-6、IL-8화TNF -α）수평승고，염성인자가이격활NF-κB，도치혈액류변학이상，사혈액처우고점、고응상태，혈류완만，역우형성혈전，인기화가속2형당뇨병합병뇌경사적발생화발전；NF-κB가작위2형당뇨병합병뇌경사환자치료중신형적약물파점。
Objective To investigate the changes of inflammatory cytokines including hs-CRP,IL-6,IL-8,TNF-α,the activity of regulatory factor-NF-κBand hemorheology in patients with type 2 diabetes mellitus complicated by cerebral infarction.Methods A parallel-controlled study was performed in the four groups including control group ( n =60),simple cerebral infarction group ( n =60),simple type 2 diabetes group( n =60),type 2 diabetes with cerebral infarction group ( n=60) .The serum levels of hs-CRP were detected by immunofluorescence assay ,the serum levels of IL6-,IL-8 and TNF-αwere measured by ELISA,and NF-κB activity was detected by immunohistochemistry .The hemorrheology parameters were detected by fully-automatic blood rheometer, and the correlation between NF-κB activity in peripheral blood of patients with type 2 diabetes mellitus complicated by cerebral infarction and hemorrheology parameters were analyzed.Results The serum levels of hs-CRP,IL-6,IL-8,TNF-αand activity of NF-κB in type 2 diabetes with cerebral infarction group were significantly higher than those in the other three groups ( P <0.01).The hemorrheology parameters in type 2 diabetes with cerebral infarction group were significantly higher than those in the other three groups ( P <0.01) .Furthermore,the activity of NF-κB in type 2 diabetes with cerebral infarction group was positively correlated to hemorrheology parameters including whole blood low-shear viscosity,highs-hear viscosity,plasma viscosity,Fib,erythrocyte aggregation index and platelet maximum aggregation rate ( P <0.01).Conclusion The levels of hs-CRP,IL-6,IL-8 and TNF-α are increased by the effect of long-term hyperglycemia, which can activate NF-κB to result in abnormal hemorheology status including high viscosity,hypercoagulability and blood flow slowing,which is easy to form thrombus and induce the pathogenesis and development of type 2 diabetes mellitus complicated by cerebral infarction.Therefore,NF-κB can be used as an new drug target in treating type 2 diabetes mellitus complicated by cerebral infarction.
