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

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

[A study on cellular matrix via cell extraction from bovine pericardium].

OBJECTIVE: To obtain an acellular matrix from bovine pericardial tissue, as a scaffold for tissue engineering of heart valves or cardiovascular patching applications. METHODS: A four step detergent and enzyme link extraction procedure was practiced in this study. The mechanic properties of the acellular matrix were evaluated, and the components were analyzed biochemically. RESULTS: HE staining confirmed the removal of cells and Von Gieson staining showed the integrality of collagen and elastin. Biochemical analysis demonstrated the retention of collagen and some glycosaminoglycans while the percentage of the soluble proteins reduced slightly. The tissue fracture strength and shrinkage temperature made no significant difference after extraction. CONCLUSIONS: The extraction process is effective to remove cells from bovine pericardial tissue while maintains its mechanical strength. This approach may eventually lead to a scaffold for heart valves and cardiovascular patching applications in tissue engineering.