临床心血管病杂志
臨床心血管病雜誌
림상심혈관병잡지
JOURNAL OF CLINICAL CARDIOLOGY
2010年
2期
130-134
,共5页
夏霓%唐婷婷%刘英%周素峰%严欣欣%朱争凤%聂少芳%刘娟%张文才%杨艳%廖玉华%程翔
夏霓%唐婷婷%劉英%週素峰%嚴訢訢%硃爭鳳%聶少芳%劉娟%張文纔%楊豔%廖玉華%程翔
하예%당정정%류영%주소봉%엄흔흔%주쟁봉%섭소방%류연%장문재%양염%료옥화%정상
心肌缺血再灌注损伤%白细胞介素-17%T淋巴细胞
心肌缺血再灌註損傷%白細胞介素-17%T淋巴細胞
심기결혈재관주손상%백세포개소-17%T림파세포
myocardial ischemia reperfusion injury%interleukin-17%T lymphocyte
目的:通过大鼠心肌缺血再灌注损伤(IRI)模型,分析白细胞介素-17(IL-17)在IRI中的作用.方法:用阻断大鼠冠状动脉左前降支的方法制作IRI模型.Real time-PCR及Western blot方法动态观察IRI后不同时间点心肌组织IL-17的表达水平,流式细胞术进一步检测IL-17的来源.应用抗IL-17抗体体内干预,观察其对IRI的作用.结果:IRI后1 h就有IL-17的表达,并且在24 h的观察期内持续存在,未有峰值出现.流式细胞术检测结果显示心肌组织中IL-17的主要来源是CD4~+T细胞.用抗IL-17的抗体体内干预后,血清肌钙蛋白T的水平降低,心肌梗死面积也明显减小.结论:IL-17参与大鼠IRI过程,中和IL-17能明显减轻心肌IRI.
目的:通過大鼠心肌缺血再灌註損傷(IRI)模型,分析白細胞介素-17(IL-17)在IRI中的作用.方法:用阻斷大鼠冠狀動脈左前降支的方法製作IRI模型.Real time-PCR及Western blot方法動態觀察IRI後不同時間點心肌組織IL-17的錶達水平,流式細胞術進一步檢測IL-17的來源.應用抗IL-17抗體體內榦預,觀察其對IRI的作用.結果:IRI後1 h就有IL-17的錶達,併且在24 h的觀察期內持續存在,未有峰值齣現.流式細胞術檢測結果顯示心肌組織中IL-17的主要來源是CD4~+T細胞.用抗IL-17的抗體體內榦預後,血清肌鈣蛋白T的水平降低,心肌梗死麵積也明顯減小.結論:IL-17參與大鼠IRI過程,中和IL-17能明顯減輕心肌IRI.
목적:통과대서심기결혈재관주손상(IRI)모형,분석백세포개소-17(IL-17)재IRI중적작용.방법:용조단대서관상동맥좌전강지적방법제작IRI모형.Real time-PCR급Western blot방법동태관찰IRI후불동시간점심기조직IL-17적표체수평,류식세포술진일보검측IL-17적래원.응용항IL-17항체체내간예,관찰기대IRI적작용.결과:IRI후1 h취유IL-17적표체,병차재24 h적관찰기내지속존재,미유봉치출현.류식세포술검측결과현시심기조직중IL-17적주요래원시CD4~+T세포.용항IL-17적항체체내간예후,혈청기개단백T적수평강저,심기경사면적야명현감소.결론:IL-17삼여대서IRI과정,중화IL-17능명현감경심기IRI.
Objective:To investigate the effect of interleukin-17(IL-17) in myocardial ischemia reperfusion injury (IRI) in rat.Method:The myocardial ischemia reperfusion injury model was performed by temporary occlusion of left anterior descending in rats. The expression of IL-17 in myocardial tissue was detected by Real time-PCR and western blot at different times after reperfusion. The source of IL -17 was confirmed by flow cytometry. Rats were treated with anti-IL-17 antibody in vivo for determining if IL -17 was involved in myocardial IRI. Result:The expression of IL-17 was detected as early as 1 hour after reperfusion, lasted for 24 hours, and showed no peak in this period. The results of flow cytometry revealed that CD4~+T lymphocyte was a major source of IL-17 in myocardial tissue after reperfusion. Administration of anti-IL-17 resulted in a significant decrease in serum troponin T and myocardial infarct size. Conclusion:IL-17 is involved in the pathogenesis of myocardial IRI.
