海南医学
海南醫學
해남의학
HAINAN MEDICAL JOURNAL
2015年
15期
2185-2188,2189
,共5页
芍药苷%心肌缺血再灌注损伤%腺苷酸活化蛋白激酶
芍藥苷%心肌缺血再灌註損傷%腺苷痠活化蛋白激酶
작약감%심기결혈재관주손상%선감산활화단백격매
Paeoniflorin%Myocardium ischemia reperfusion injury%AMP-activated protein kinase alpha (AMPKα)
目的：探究芍药苷预处理激活AMPKα信号通路对大鼠在体心肌缺血再灌注损伤的保护作用。方法本实验共用SPF级雄性SD大鼠30只，分三组，分别为假手术组、缺血再灌注组、药物预处理组，采用结扎SD大鼠心脏LAD的方法建立在体大鼠心肌缺血再灌注损伤模型，利用0.5%Evan's蓝灌注心肌，1%氯化三苯基四氮唑(TTC)磷酸缓冲液孵育心肌，CK-MB试剂盒来观察心肌缺血、坏死及肌酸磷酸激酶(CK-MB)和HE染色观察心肌损伤程度，利用蛋白印迹(Western blot)技术探究芍药苷预处理对腺苷酸活化蛋白激酶(AMPKα)的影响。结果芍药苷药物预处理组与缺血再灌注组比较，药物预处理组心梗面积较缺血再灌注组明显减小(P<0.01)；CK-MB检测也发现药物预处理组与缺血再灌注组比较能明显降低CK-MB值(P<0.01)；HE染色发现药物预处理组较缺血再灌注组能明显减轻大鼠心肌局灶性肿胀、心肌间质水肿，减少炎性细胞浸润及血管充血；蛋白印迹实验发现药物预处理组能明显促进AMPKα蛋白的表达，升高磷酸化AMPKα的表达。结论芍药苷预处理能减轻大鼠在体心肌缺血再灌注损伤，可能通过增加AMPKα蛋白的表达，促进AMPKα磷酸化而实现。
目的：探究芍藥苷預處理激活AMPKα信號通路對大鼠在體心肌缺血再灌註損傷的保護作用。方法本實驗共用SPF級雄性SD大鼠30隻，分三組，分彆為假手術組、缺血再灌註組、藥物預處理組，採用結扎SD大鼠心髒LAD的方法建立在體大鼠心肌缺血再灌註損傷模型，利用0.5%Evan's藍灌註心肌，1%氯化三苯基四氮唑(TTC)燐痠緩遲液孵育心肌，CK-MB試劑盒來觀察心肌缺血、壞死及肌痠燐痠激酶(CK-MB)和HE染色觀察心肌損傷程度，利用蛋白印跡(Western blot)技術探究芍藥苷預處理對腺苷痠活化蛋白激酶(AMPKα)的影響。結果芍藥苷藥物預處理組與缺血再灌註組比較，藥物預處理組心梗麵積較缺血再灌註組明顯減小(P<0.01)；CK-MB檢測也髮現藥物預處理組與缺血再灌註組比較能明顯降低CK-MB值(P<0.01)；HE染色髮現藥物預處理組較缺血再灌註組能明顯減輕大鼠心肌跼竈性腫脹、心肌間質水腫，減少炎性細胞浸潤及血管充血；蛋白印跡實驗髮現藥物預處理組能明顯促進AMPKα蛋白的錶達，升高燐痠化AMPKα的錶達。結論芍藥苷預處理能減輕大鼠在體心肌缺血再灌註損傷，可能通過增加AMPKα蛋白的錶達，促進AMPKα燐痠化而實現。
목적：탐구작약감예처리격활AMPKα신호통로대대서재체심기결혈재관주손상적보호작용。방법본실험공용SPF급웅성SD대서30지，분삼조，분별위가수술조、결혈재관주조、약물예처리조，채용결찰SD대서심장LAD적방법건립재체대서심기결혈재관주손상모형，이용0.5%Evan's람관주심기，1%록화삼분기사담서(TTC)린산완충액부육심기，CK-MB시제합래관찰심기결혈、배사급기산린산격매(CK-MB)화HE염색관찰심기손상정도，이용단백인적(Western blot)기술탐구작약감예처리대선감산활화단백격매(AMPKα)적영향。결과작약감약물예처리조여결혈재관주조비교，약물예처리조심경면적교결혈재관주조명현감소(P<0.01)；CK-MB검측야발현약물예처리조여결혈재관주조비교능명현강저CK-MB치(P<0.01)；HE염색발현약물예처리조교결혈재관주조능명현감경대서심기국조성종창、심기간질수종，감소염성세포침윤급혈관충혈；단백인적실험발현약물예처리조능명현촉진AMPKα단백적표체，승고린산화AMPKα적표체。결론작약감예처리능감경대서재체심기결혈재관주손상，가능통과증가AMPKα단백적표체，촉진AMPKα린산화이실현。
Objective To explore the protective effects of pretreatment with paeoniflorin on the myocardial ischemia reperfusion injury of rats in vivo by activating AMPKα. Methods The SPF grade male SD rats (30 rats) were divided into three groups: sham operation group [the rats' chests were opened, but the left anterior descending coronary arteries (LAD) were not ligated], ischemia reperfusion group and paeoniflorin pretreatment group, each with 10 cases. Myocardial ischemia reperfusion injury model was established by cardiac LAD ligation in SD rats. The de-gree of myocardial injury was observed by HE staining and perfusion of 0.5%Evan's blue and 1%triphenyl tetrazoli-um chloride (TTC). Western blot was used to explore the effects of paeoniflorin pretreatment on AMPKα. Results In comparison with ischemic reperfusion group, paeoniflorin pretreatment could decrease infarction area significantly (P<0.01) and reduce the value of creatine phosphokinase (CK-MB) significantly (P<0.01). HE staining showed paeoniflo-rin pretreatment could significantly relieve myocardial focal swelling, intermyocardial swelling, inflammatory cell in-filtration, and vascular engorgement. Western blot showed that paeoniflorin pretreatment could increase the expression of AMPKαand promote the phosphorylation of AMPKα. Conclusion Pretreatment with paeoniflorin could relieve myocardial ischemia reperfusion injury of rats in vivo. The effect is probably achieved by increasing the expression of AMPKαand promoting phosphorylation of AMPKα.
