青岛大学医学院学报
青島大學醫學院學報
청도대학의학원학보
ACTA ACADEMIAE MEDICINAE QINGDAO UNIVERSITATIS
2008年
2期
129-132
,共4页
心肌%缺血后处理%RISK信号转导通路%再灌注损伤%肠系膜上动脉
心肌%缺血後處理%RISK信號轉導通路%再灌註損傷%腸繫膜上動脈
심기%결혈후처리%RISK신호전도통로%재관주손상%장계막상동맥
Myocardium%Ischemic postconditioning%RISK pathway%Reperfusion injury%The superior mesenteric artery
目的通过在体兔心肌缺血再灌注模型, 研究再灌注损伤补救酶(reperfusion injury salvage kinase,RISK)信号转导通路是否参与肠系膜上动脉缺血后处理对急性心肌缺血再灌注损伤的保护作用.方法 32只兔随机分为缺血再灌注组(IR组),肠系膜上动脉缺血后处理组(MIPostC组),缺血预处理+肠系膜上动脉缺血后处理组(IPC +MIPostC组),药物干预+肠系膜上动脉缺血后处理组(DI+ MIPostC组),每组8只.实验达终点时,取结扎血管支配部位心肌测定心肌梗死面积并观察心肌细胞超微结构改变;利用Westernblot技术检测各组动物心肌蛋白激酶B(Akt)、内皮型一氧化氮合酶(eNOS)蛋白磷酸化的表达.结果 MIPostC组和IPC+MIPostC组坏死面积占总面积之比均明显低于其他组(F=4.72,q=3.69～4.20,P<0.05);而二者之间相比,坏死面积占总面积之比无明显差别(P>0.05) ; DI + MIPostC组LY294002消除了缺血后处理的上述减少心肌梗死面积的作用(q=4.18,P<0.05).MIPostC组Akt和eNOS蛋白表达明显高于IR和DI + MIPostC 组(F=276.34、31.8,q=9.02～29.82,P<0.01); DI + MIPostC组LY294002消除了缺血后处理减轻再灌注损伤作用.结论 心肌缺血再灌注时立即行肠系膜上动脉缺血后处理与心肌缺血预处理共同运用并不能产生额外的心脏保护作用; RISK信号转导通路参与肠系膜上动脉缺血后处理对急性心肌缺血再灌注损伤的保护作用.
目的通過在體兔心肌缺血再灌註模型, 研究再灌註損傷補救酶(reperfusion injury salvage kinase,RISK)信號轉導通路是否參與腸繫膜上動脈缺血後處理對急性心肌缺血再灌註損傷的保護作用.方法 32隻兔隨機分為缺血再灌註組(IR組),腸繫膜上動脈缺血後處理組(MIPostC組),缺血預處理+腸繫膜上動脈缺血後處理組(IPC +MIPostC組),藥物榦預+腸繫膜上動脈缺血後處理組(DI+ MIPostC組),每組8隻.實驗達終點時,取結扎血管支配部位心肌測定心肌梗死麵積併觀察心肌細胞超微結構改變;利用Westernblot技術檢測各組動物心肌蛋白激酶B(Akt)、內皮型一氧化氮閤酶(eNOS)蛋白燐痠化的錶達.結果 MIPostC組和IPC+MIPostC組壞死麵積佔總麵積之比均明顯低于其他組(F=4.72,q=3.69～4.20,P<0.05);而二者之間相比,壞死麵積佔總麵積之比無明顯差彆(P>0.05) ; DI + MIPostC組LY294002消除瞭缺血後處理的上述減少心肌梗死麵積的作用(q=4.18,P<0.05).MIPostC組Akt和eNOS蛋白錶達明顯高于IR和DI + MIPostC 組(F=276.34、31.8,q=9.02～29.82,P<0.01); DI + MIPostC組LY294002消除瞭缺血後處理減輕再灌註損傷作用.結論 心肌缺血再灌註時立即行腸繫膜上動脈缺血後處理與心肌缺血預處理共同運用併不能產生額外的心髒保護作用; RISK信號轉導通路參與腸繫膜上動脈缺血後處理對急性心肌缺血再灌註損傷的保護作用.
목적통과재체토심기결혈재관주모형, 연구재관주손상보구매(reperfusion injury salvage kinase,RISK)신호전도통로시부삼여장계막상동맥결혈후처리대급성심기결혈재관주손상적보호작용.방법 32지토수궤분위결혈재관주조(IR조),장계막상동맥결혈후처리조(MIPostC조),결혈예처리+장계막상동맥결혈후처리조(IPC +MIPostC조),약물간예+장계막상동맥결혈후처리조(DI+ MIPostC조),매조8지.실험체종점시,취결찰혈관지배부위심기측정심기경사면적병관찰심기세포초미결구개변;이용Westernblot기술검측각조동물심기단백격매B(Akt)、내피형일양화담합매(eNOS)단백린산화적표체.결과 MIPostC조화IPC+MIPostC조배사면적점총면적지비균명현저우기타조(F=4.72,q=3.69～4.20,P<0.05);이이자지간상비,배사면적점총면적지비무명현차별(P>0.05) ; DI + MIPostC조LY294002소제료결혈후처리적상술감소심기경사면적적작용(q=4.18,P<0.05).MIPostC조Akt화eNOS단백표체명현고우IR화DI + MIPostC 조(F=276.34、31.8,q=9.02～29.82,P<0.01); DI + MIPostC조LY294002소제료결혈후처리감경재관주손상작용.결론 심기결혈재관주시립즉행장계막상동맥결혈후처리여심기결혈예처리공동운용병불능산생액외적심장보호작용; RISK신호전도통로삼여장계막상동맥결혈후처리대급성심기결혈재관주손상적보호작용.
Objective To study whether the reperfusion injury salvage kinase (RISK) pathway take part in cardioprotection of superior mesenteric artery ischemic postconditioning on rabbit cardiac ischemia-reperfusion model in vivo. Methods The rabbits were randomly divided into the following group (eight in each group): Ischemia-reperfusion (IR); superior mesenteric artery ischemic postconditioning (MI-PostC); ischemic preconditioning (IPC)+ MI-PostC; drug intervention (DI) + MI-PostC. When the experiment completed,the heart in each group was harvested and dyed with NBT (nitroblue tetrazolium), the infarct size determined. The tissue structures were observed microscopically. Myocardium Akt and eNOS were tested by Western-blot methods. Results Infarct size was significantly less in the MI-PostC and IPC+MI-PostC groups than that of the other groups (F=4.72,q=3.69-4.20,P<0.05), but there were no differences between this two groups.However, in DI +MI-PostC groups, LY294002 abrogated the myocardium infarct size reduction in MI-PostC group (q=4.18,P<0.05). The quantity of Akt and eNOS in myocardium was higher in MI-PostC than in the other groups (F=276.34,31.8;q=9.02-29.82;P<0.01). Similarly,in DI +MI-PostC group, LY294002 abolished this protective effect in MI-PostC group. Conclusion When reperfusion is done for the ischemic myocardium, superior mesenteric artery ischemic postconditioning can not produce supernumerary protection on the base of ischemic preconditioning. RISK pathway takes part in cardioprotection of superior mesenteric artery ischemic postconditioning.
