【摘要】：研究七氟烷后處理對在體大鼠心肌缺血再灌注(I/R)損傷的保護作用,探討腺苷酸活化蛋白激酶(AMPK)介導(dǎo)的自噬流在七氟烷后處理心肌保護中的作用。成年雄性SD大鼠50只,建立急性大鼠在體心肌I/R損傷模型。隨機分為5組:假手術(shù)組(Sham組)、缺血再灌注組(I/R組)、七氟烷后處理組(SP組)、Compound c溶劑二甲基亞砜組(DMSO組)、AMPK抑制劑Compound c組(Com c組)。除Sham組,其余各組缺血30 min,再灌注4 h末。再灌注4 h末,提取心臟,采用氯化三苯基四氮唑染色法(TTC法)測定心肌梗死范圍。采用免疫印跡法(Western blot技術(shù))檢測p-AMPK/t-AMPK、LC3Ⅱ/Ⅰ及P62蛋白表達水平。與I/R組比較,SP組心肌梗死范圍減小,p-AMPK/t-AMPK蛋白表達上調(diào)而LC3Ⅱ/Ⅰ、P62蛋白表達下調(diào)(P0.05);與SP組比較,Com c組心肌梗死范圍增加,p-AMPK/t-AMPK蛋白表達下調(diào)而LC3Ⅱ/Ⅰ、P62蛋白表達上調(diào)(P0.05)。DMSO組相比于SP組差別無統(tǒng)計學(xué)意義(P0.05)。七氟烷后處理減輕了在體大鼠心肌I/R損傷,其機制可能是通過激活A(yù)MPK信號通路,減少再灌注期間自噬體的蓄積,保護自噬流進而發(fā)揮保護作用。
[Abstract]:To investigate the protective effect of sevoflurane post-treatment on myocardial ischemia-reperfusion (I-R) injury in rats, and to explore the role of adenylate-activated protein kinase (AMPK)-mediated autophagy flow in myocardial protection after sevoflurane treatment. Acute myocardial I R injury model was established in 50 adult male SD rats. They were randomly divided into 5 groups: sham-operation group (Sham group), ischemia-reperfusion group (I-R group) and sevoflurane post-treatment group (SP group), Compound c solvent dimethyl sulfoxide group (DMSO group), AMPK inhibitor Compound c (Com c group). With the exception of Sham group, the other groups were subjected to ischemia for 30 min, at the end of 4 h. At the end of 4 h reperfusion, the heart was extracted and the infarct size was measured by TTC method. The expression levels of pAMPK, LC3 鈪，

本文編號：2438113