Effect of propofol on myocardial ischemia-reperfusion injury through MAPK/ERK pathway.

Myocardial Reperfusion Injury
DOI: 10.26355/eurrev_201912_19813 Publication Date: 2019-12-01
ABSTRACT
The aim of this study was to investigate the effects propofol on myocardial ischemia-reperfusion injury (MIRI) and mitogen-activated protein kinase (MAPK)/extracellular signal-regulated (ERK) pathway. Primary cells were first isolated from rats. apoptosis primary expression apoptosis-related proteins detected via flow cytometry Western blotting, respectively. Meanwhile, effect MIRI model after ischemia for 2 h reperfusion 24 as well. Subsequently, activity in tissues using transcriptome sequencing VIPER method. 2, 3, 5- triphenyl tetrazolium chloride (TTC) staining, hematoxylin-eosin (HE) Masson staining. Besides, function BL-420F hemodynamic system. Propofol MAPK/ERK signaling pathway determined blotting vivo. Finally, content serum lactate dehydrogenase (LDH), creatine (CK), total superoxide dismutase (T-SOD), malondialdehyde (MDA) relevant kits. activated a dose-dependent manner cells, which also reduced apoptotic rate cells. results TTC HE staining showed that significantly ERK inhibitor PD-98059 could reduce cardioprotective propofol. decreased LDH, CK, MDA (p<0.05), while it increased T-SOD (p<0.05). According study, statistically significant differences observed left ventricular systolic pressure (LVSP), maximal decrease (-dp/dtmax), end-diastolic (LVEDP) between group (p<0.01). revealed level p-ERK1/2 dose-and time-dependent Furthermore, remarkably at 8 ischemia-reperfusion. exerts cardio-protective through
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