Endothelial Cells ; Fibrosis ; Humans ; Mesenchymal Stromal Cells ; Myocardium ; pathology

Objective To investigate the expression and significance of activator protein-1 (AP-1)and matrix metalloproteinases (MMPs) in acute myocardial infarction (AMI) subjects. Methods Immunohistochemical techniques were used to detect the subunit of AP-1 (c-Jun), MMP-2 and MMP-9 in human AMI and normal heart tissue and the expressions of c-Jun and MMPs were measured with computer image analysis system. Results (1) There were expressions of c-Jun, MMP-2 and MMP-9 in normal heart tissue, mainly in myocardial cells and cardiac fibroblasts, and their expressions in AMI myocardial tissues were all significantly higher than those in normal myocardial tissues (P <0.05). (2) The level of MMP-9expression was significantly and positively correlated with c-Jun in AMI heart tissue (r=0.773, P < 0.01).Conclusions The expressions of AP-1 and MMPs increase in human myocardial infarction. These findings suggest that AP-1 transcription activation pathway and MMPs may play an important role in ventricular remodeling of myocardial infarction.

AIM: The aim of this study was to investigate the possibility of establishing a chronic atrial fibrillation model with long-term rapid atrial stimulation ( 1 000 bpm), which was performed in rabbits in vivo. METHODS: 20 rabbits were randomly divided into 2 groups: 1) control group (n=10): pacemaker was implanted but no pacing; 2) experimental group (n=10): a left intercostal thoracotomy was performed and the pericardium was opened to expose the heart and a steel-wire pacing electrode was fixed on the epicardium of the left atria in 10 rabbits. Then the rapid pulse generator was implanted subcutaneously in the left abdominal region and rapid atrial pacing ( 1 000 beats/min) was initiated and continued for 30 days. Electrocardiogram (ECG) was monitored and recorded on day 1, 3, 5, 7, 14, 21 and 30. The atrial effective refractory period (AERP) was measured before pacing and at the time of fibrillation. RESULTS: On day 14, atrial fibrillation was developed in 8 rabbits (80%) and sustained at least till to day 30 (P

AIM:To investigate the effects of ox-LDL on TLR2 and TLR4 expression and production of TNF-?,IL-10,IL-12,NO and MDA in macrophages and to observe intervention effect of GW1929 in above procedure.METHODS:The mouse peritoneal macrophages were pretreated with ox-LDL(50 mg/L,100 mg/L)and GW1929(20 ?mol/L)respectively for 24 h.The concentrations of MDA,NO-2/NO-3,TNF-?,IL-10 and IL-12 in the culture fluid were detected.Flow cytometry was used to observe TLR2 and TLR4 expressions after the mouse peritoneal macrophages were pretreated with ox-LDL(50 mg/L)and GW1929(20 ?mol/L)respectively for 6 h,12 h,and 24 h.RESULTS:The concentrations of MDA,NO-2/NO-3,TNF-? and IL-10 in ox-LDL(50 mg/L,100 mg/L)group were higher than those in control and GW1929 group obviously,but the concentrations of above index in ox-LDL(50 mg/L,100 mg/L)+GW1929 group were lower than those in ox-LDL(50 mg/L,100 mg/L)group apparently.No IL-12 in every group was detected.Expressions of TLR-2 in ox-LDL+GW1929(6 h,12 h,24 h)group were lower than those in ox-LDL(6 h,12 h,24 h)group respectively.TLR-4 expressions in ox-LDL+GW1929(12 h)were lower than those in ox-LDL(12 h)apparently.CONCLUSION:ox-LDL up-regulates TLR2 and TLR4 expressions and promotes the production of ROX,NO,TNF-? and IL-10 in macrophages.GW1929 is capable of inhibiting the above ox-LDL effects.