重庆医学
重慶醫學
중경의학
CHONGQING MEDICAL JOURNAL
2013年
36期
4427-4429
,共3页
高建芝%赵林静%张婧君%腾清蕾
高建芝%趙林靜%張婧君%騰清蕾
고건지%조림정%장청군%등청뢰
缺血预处理%心肌再灌注损伤%脂联素%脂联素受体1%信号转导%细胞凋亡
缺血預處理%心肌再灌註損傷%脂聯素%脂聯素受體1%信號轉導%細胞凋亡
결혈예처리%심기재관주손상%지련소%지련소수체1%신호전도%세포조망
ischemic preconditioning reperfusion injury%myocardium%adiponectin%receptor1%apoptosis
目的:研究脂联素(ADP)及其受体在缺血预适应(LIPC)抗缺血、再灌注(MIRI)大鼠心肌细胞凋亡中的作用。方法雄性SD大鼠分为3组(n=10,每组4只备用于细胞凋亡):假手术(sham组):左冠状动脉前降支仅穿线不处理;M IRI组:左前降支缺血30 min ,再灌注120 min;LIPC组:肢体缺血5 min ,再灌注5 min ,连续预适应3 d后实施缺血30 min ,再灌注120 min。采用逆转录聚合酶链式反应(RT-PCR)法和原位末端缺口标记(TUNEL)法检测各组心肌组织 ADP和ADP受体1(ADPR1)的mRNA表达和心肌细胞的凋亡指数。结果与 sham组相比,MIRI组ADP和ADPR1的mRNA表达明显减少(P<0.05);与MIRI组相比,LIPC组ADP和ADPR1的mRNA表达上调,差异有统计学意义(P<0.05);MIRI组大鼠心肌细胞的凋亡指数(AI)比sham组增加显著,差异有统计学意义(P<0.05);与MIRI组相比,LIPC组心肌细胞的AI明显减少,差异有统计学意义(P<0.05)。结论 LIPC可能通过ADP信号通路减轻心肌-再灌注损伤后的细胞凋亡,发挥其心肌保护作用。
目的:研究脂聯素(ADP)及其受體在缺血預適應(LIPC)抗缺血、再灌註(MIRI)大鼠心肌細胞凋亡中的作用。方法雄性SD大鼠分為3組(n=10,每組4隻備用于細胞凋亡):假手術(sham組):左冠狀動脈前降支僅穿線不處理;M IRI組:左前降支缺血30 min ,再灌註120 min;LIPC組:肢體缺血5 min ,再灌註5 min ,連續預適應3 d後實施缺血30 min ,再灌註120 min。採用逆轉錄聚閤酶鏈式反應(RT-PCR)法和原位末耑缺口標記(TUNEL)法檢測各組心肌組織 ADP和ADP受體1(ADPR1)的mRNA錶達和心肌細胞的凋亡指數。結果與 sham組相比,MIRI組ADP和ADPR1的mRNA錶達明顯減少(P<0.05);與MIRI組相比,LIPC組ADP和ADPR1的mRNA錶達上調,差異有統計學意義(P<0.05);MIRI組大鼠心肌細胞的凋亡指數(AI)比sham組增加顯著,差異有統計學意義(P<0.05);與MIRI組相比,LIPC組心肌細胞的AI明顯減少,差異有統計學意義(P<0.05)。結論 LIPC可能通過ADP信號通路減輕心肌-再灌註損傷後的細胞凋亡,髮揮其心肌保護作用。
목적:연구지련소(ADP)급기수체재결혈예괄응(LIPC)항결혈、재관주(MIRI)대서심기세포조망중적작용。방법웅성SD대서분위3조(n=10,매조4지비용우세포조망):가수술(sham조):좌관상동맥전강지부천선불처리;M IRI조:좌전강지결혈30 min ,재관주120 min;LIPC조:지체결혈5 min ,재관주5 min ,련속예괄응3 d후실시결혈30 min ,재관주120 min。채용역전록취합매련식반응(RT-PCR)법화원위말단결구표기(TUNEL)법검측각조심기조직 ADP화ADP수체1(ADPR1)적mRNA표체화심기세포적조망지수。결과여 sham조상비,MIRI조ADP화ADPR1적mRNA표체명현감소(P<0.05);여MIRI조상비,LIPC조ADP화ADPR1적mRNA표체상조,차이유통계학의의(P<0.05);MIRI조대서심기세포적조망지수(AI)비sham조증가현저,차이유통계학의의(P<0.05);여MIRI조상비,LIPC조심기세포적AI명현감소,차이유통계학의의(P<0.05)。결론 LIPC가능통과ADP신호통로감경심기-재관주손상후적세포조망,발휘기심기보호작용。
Objective To evaluate the role of adiponectin (ADP) and adiponectin receptor-1(ADPR1) in limb ischemic precondi-tioning(LIPC) against apoptosis after myocardial ischemia-reperfusion injury(MIRI) .Methods SD rats were divided into 3 groups (n=10 ,4 rats of every group were prepared for detecting apoptosis ) .Group sham (group in sham operated) were processed identi-cally except the left coronary artery was not be ligated ;group MIRI (group in ischemia reperfusion) were subjected to occlusion of the left coronary artery anterior descending (LAD) followed by reperfusion ,occlusion for 30 min and reperfusion for 120 min;group LIPC (group in limb ischemic preconditioning) were subjected to ischemia and reperfusion on the left hind limb for 5 min in turn for 3 d .LAD were performed ischemia for 30 min and reperfusion for 120 min at the 4th day .The expression of the level of myocardial ADP and ADPR1 mRNA of group sham ,group MIRI and group LIPC were determined by reverse transcriptase polymerase chain reaction(RT-PCR) .The apoptosis index of every group were determined by mothod of terminal-deoxynucleoitidyl transferase medi-ated nick end labeling(TUNEL)respectively .Results Compared with group sham ,the expression of ADP and ADPR1 mRNA in group MIRI lessened apparently (P<0 .05);compared with group MIRI ,the expression of ADP and ADPR1 mRNA in group LIPC increased statistically significant(P<0 .05);compared with group sham ,the apoptosis index(AI) of myocardial cells in group MIRI increased apparently(P<0 .05);compared with group MIRI ,the AI of myocardial cells in group LIPC decreased significantly (P<0 .05) .Conclusion Limb ischemic preconditioning ;decreased apoptosis after myocardial ischemia-reperfusion injury via activating ADP signaling pathways ,which played a protective role in myocardial tissue .