重庆医学
重慶醫學
중경의학
CHONGQING MEDICAL JOURNAL
2014年
15期
1901-1903
,共3页
再灌注损伤%NF-κB%血管紧张素Ⅱ%吡咯烷二硫基甲酸酯%咪达普利
再灌註損傷%NF-κB%血管緊張素Ⅱ%吡咯烷二硫基甲痠酯%咪達普利
재관주손상%NF-κB%혈관긴장소Ⅱ%필각완이류기갑산지%미체보리
reperfusion injury%NF-kappa B%angiotensinⅡ%pyrrolidine dithiocarbamate%imidapril
目的：初步探讨心肌缺血再灌注损伤（IRI）过程中NF‐κBp65与血管紧张素Ⅱ（AngⅡ）的关系。方法建立在体大鼠心肌IRI模型。以缺血30 min再灌注60 min（I30 min R60 min ）为观察点，采用随机数字表法分为IR组（即I30 min R60 min后不再经任何处理）、PDTC预处理组、咪达普利预处理组、PDTC与咪达普利联合预处理组。分别通过酶联免疫吸附试验（ELISA）及放射免疫分析法检测NF‐κBp65活性及血浆和心肌组织中的AngⅡ含量。通过析因分析观察NF‐κBp65与AngⅡ的相关性。结果各药物预处理组与IR组比均可抑制NF‐κBp65活性及血浆和心肌组织中的AngⅡ含量，差异有统计学意义（P＜0．05）。结论心肌缺血再灌注损伤过程中NF‐κBp65与AngⅡ相互激活，形成正反馈，共同加重此损伤病理过程。
目的：初步探討心肌缺血再灌註損傷（IRI）過程中NF‐κBp65與血管緊張素Ⅱ（AngⅡ）的關繫。方法建立在體大鼠心肌IRI模型。以缺血30 min再灌註60 min（I30 min R60 min ）為觀察點，採用隨機數字錶法分為IR組（即I30 min R60 min後不再經任何處理）、PDTC預處理組、咪達普利預處理組、PDTC與咪達普利聯閤預處理組。分彆通過酶聯免疫吸附試驗（ELISA）及放射免疫分析法檢測NF‐κBp65活性及血漿和心肌組織中的AngⅡ含量。通過析因分析觀察NF‐κBp65與AngⅡ的相關性。結果各藥物預處理組與IR組比均可抑製NF‐κBp65活性及血漿和心肌組織中的AngⅡ含量，差異有統計學意義（P＜0．05）。結論心肌缺血再灌註損傷過程中NF‐κBp65與AngⅡ相互激活，形成正反饋，共同加重此損傷病理過程。
목적：초보탐토심기결혈재관주손상（IRI）과정중NF‐κBp65여혈관긴장소Ⅱ（AngⅡ）적관계。방법건립재체대서심기IRI모형。이결혈30 min재관주60 min（I30 min R60 min ）위관찰점，채용수궤수자표법분위IR조（즉I30 min R60 min후불재경임하처리）、PDTC예처리조、미체보리예처리조、PDTC여미체보리연합예처리조。분별통과매련면역흡부시험（ELISA）급방사면역분석법검측NF‐κBp65활성급혈장화심기조직중적AngⅡ함량。통과석인분석관찰NF‐κBp65여AngⅡ적상관성。결과각약물예처리조여IR조비균가억제NF‐κBp65활성급혈장화심기조직중적AngⅡ함량，차이유통계학의의（P＜0．05）。결론심기결혈재관주손상과정중NF‐κBp65여AngⅡ상호격활，형성정반궤，공동가중차손상병리과정。
Objective Utilizing the characters of pyrrolidine dithiocarbamate known as a specific inhibitor of NF‐κB and imidapril known as a specific inhibitor of angiotensin converting enzyme ,this study was to initially investigate the relationship between NF‐κBp65 and AngⅡ during the process of myocardial ischemia reperfusion injury .Methods Rat models of myocardial ischemia reper‐fusion injury were successfully established .The observation point is 60 min of reperfusion after 30 min(I30 min R60 min ) ischemia ,the DNA activate of NF‐κBp65 was detected by ELISA ;the content of AngⅡ in blood plasma and cardiac were determined by radioim‐munoassay .We pretreated with pyrrolidine dithiocarbamate ,imidapril ,and both of them to observe changes of the same indexs .Re‐sults Compared with I30 min R60 min ,Pyrrolidine dithiocarbamate ,Imidapril and pyrrolidine dithiocarbamate add imidapril could all ob‐viously inhibit NF‐κBp65 activation and depress the content of Ang Ⅱ in blood plasm and cardiac ,the pyrrolidine dithiocarbamate add imidapril was most obviously .Conclusion During the process of myocardial ischemia‐reperfusion injury ,NF‐κBp65 had been activated ,and the content of Ang Ⅱ in blood plasm and cardiac had increased .NF‐κBp65 and AngⅡ could influence and promote each other during myocardial ischemia reperfusion injury .
