摘要
目的探讨环泊酚改善心肌缺血再灌注大鼠心肌损伤的作用机制。方法将30只大鼠随机分为假手术组、模型组与环泊酚组,采用左冠状动脉前降支结扎法建立心肌缺血再灌注损伤模型。超声检测大鼠心脏功能;三苯基氯化四氮唑(TTC)染色检测各组大鼠心肌梗死面积;酶联免疫吸附实验(ELISA)检测各组大鼠血清中磷酸肌酸激酶同工酶(CK-MB)、肌钙蛋白I(cTnI)水平;试剂盒检测心肌组织丙二醛(MDA)、超氧化物歧化酶(SOD)及谷胱甘肽(GSH)水平;比色法检测大鼠心肌组织中Fe2+含量;普鲁士蓝染色法检测心肌组织铁离子的聚集情况;Western blot法检测各组大鼠心肌组织谷胱甘肽过氧化物酶4(GPX4)、溶质载体家族7成员11(SLC7A11)蛋白表达。结果环泊酚干预后,大鼠LVEF%、FS%显著升高,LVEDD、LVESD显著降低,心肌梗死面积显著减小,CK-MB、cTnI水平显著降低,MDA含量降低,SOD、GSH水平升高,Fe2+含量和铁离子聚集降低,GPX4、SLC7A11蛋白表达水平显著升高。结论环泊酚可改善心肌缺血再灌注大鼠心肌损伤,减少心肌组织铁沉积,其作用机制可能与调控GPX4/SLC7A11通路,抑制铁死亡有关。
Objective To investigate the mechanism of ciprofol in improving myocardial injury in rats with myocardial ischemia and reperfusion.Methods Thirty rats were randomly divided into three groups,namely sham,model and ciprofol group.The left anterior descending coronary artery ligation method was used to establish a model of myocardial ischemia-reperfusion injury.Rats were tested for cardiac function by ultrasound.The area of myocardial infarction in rats was measured by triphenyltetrazolium chloride(TTC)staining.The levels of phosphocreatine kinase isoenzyme(CK-MB)and troponin I(cTnI)in serum of rats were detected by enzyme-linked immunosorbent assay(ELISA).Malondialdehyde(MDA),superoxide dismutase(SOD)and glutathione(GSH)levels and Fe~(2+)content in myocardial tissue of rats were detected.The concentration of iron in myocardial tissue was detected by prussian blue staining.The expressions of glutathione peroxidase 4(GPX4)and solute carrier family 7 member 11(SLC7A11)in myocardial tissue of rats were detected by Western blot.Results After ciprofol intervention,LVEF%and FS%were significantly increased,LVEDD and LVESD were significantly decreased,myocardial infarction area was significantly reduced,levels of CK-MB and cTnI were significantly reduced,content of MDA was reduced,levels of SOD and GSH were increased,content of Fe~(2+)and iron accumulation were decreased,and the expressions of GPX4 and SLC7A11 protein were significantly increased.Conclusion Ciprofol can improve myocardial injury and reduce myocardial tissue iron deposition in myocardial ischemia-reperfusion rats,and its mechanism may be related to the regulation of GPX4/SLC7A11 pathway and inhibition of ferroptosis.
作者
张良
刘雁
孙妍
王维维
周南
程芳
ZHANG Liang;LIU Yan;SUN Yan;WANG Wei-wei;ZHOU Nan;CHENG Fang(Department of Anesthesiology,Dalian Central Hospital,Dalian 116089;Department of Anesthesiology,Northern Theater Command General Hospital,Shenyang 110016,China)
出处
《解剖科学进展》
CAS
2024年第2期205-208,共4页
Progress of Anatomical Sciences
基金
辽宁省自然科学基金(20180551091)。