| Objective:In this study, we use a model of ischemia-reperfusion(I/R) on isolated rat heartto observe the influence of liver X receptors (LXRs) on myocardialischemia-reperfusion (I/R) injury.To investigate whether LXRs attenuate myocardialischemia reperfusion induced injury in isolated rat heart through modulating Glucosetransporter4(GLUT4).Methods:1. Isolated rat hearts were used to establishing ischemia-reperfusion injuy modelthrough using Langendorff apparatus:Isolated rat hearts were exposed to30min ofglobal ischemia followed by120min of reperfusion.2. Hearts were divided into seven groups:①control group:perfused with nomalK-H buffer.②control+DMSO group: pretreatment with0.02%DMSO.③I/R group:Isolated rat hearts were exposed to30min of global ischemia followed by120min ofreperfusion.④pretreatment with0.1μmol/L T0901317（Liver X receptor agonist）⑤pretreatment with0.1μmol/L T0901317,⑥pretreatment with0.5μmol/LT0901317.⑦ischemic preconditioning group;3. Ischemia Myocardial injury was assessed in the terms of infarct size using thetriphenyltetrazolium chloride （TTC） staining technique, release of lactatedehydrogenase (LDH) and creatine kinase (CK) enzymes were detected bycolorimetry.4. The following parameters were monitored by using multipurpose polygraph:LVEDP,LVDP,±dp/dtmaxand coronary flow rat.5. The relative transcription level of GLUT-4was quantified by quantitativereal-time PCR. The content of GLUT-4in myocardial cell membrane was detected byusing Western blot.Results:1.In the model groups, the LDH,CK activity and infarct size were increased afterischemia reperfusion (P <0.05), besides produce hemodynamic disorders: CF, LVDP, ±dp/dtmax were decreased significantly (P <0.05), and LVEDP were increasedsignificantly (P <0.05).But control+DMSO group did not change significantly.2.Treatment with T0901317and IPC significantly suppressed ischemiareperfusion injury induced increases in LDH and CK,also reduced the infarct sizeconspicuous (P＜0.05).3. Treatment with T0901317and IPC significantly significantly amelioratedparameters of haemodynamics: CF, LVDP,±dp/dtmax were increased (P <0.05),and LVEDP were decreased (P <0.05) compared to the I/R group.4. Treatment with T0901317and IPC significantly increased GLUT-4expressionat mRNA level and the content of GLUT-4protein in myocardial cell membrane.Conclusion:1．LXRs could reduce the myocardial I/R injury on isolated rat heart.2. LXRs may attenuate myocardial ischemia reperfusion injury in isolated ratheart by modulating GLUT-4. |
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