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Aim To investigate the effects of total gin-senosides ( TG) on microvascular regeneration and car-diac function in rat after acute myocardial infarction ( AMI ) . Methods The acute myocardial infarction model was created with left coronary artery ligated in male Sprague Dawley rats. The model rats were ran-domly divided into sham, model, TG low and high dose groups. TG groups were injected into abdominal cavity with TG(20 mg·kg-1·d-1, 40 mg·kg-1· d-1 ) . Sham and model groups were injected with e-qual-volume normal saline. On the 35th day post-opera-tion, heart function was examined by color doppler ul-trasoundination. HE, Masson and immunohistochemis-trical staining were used to observe the histopathologi-cal changes of myocardium and micro vessel density. The level of vascular endothelial growth factor( VEGF) and basic fibroblast growth factor( bFGF) mRNA were detected by real-time PCR. Results Compared with the model group, high and low dose TG obviously de-creased the left ventricular end diastolic dimension, the left ventricular end-systolic dimension, the left ventric-ular end-diastolic volume and the left ventricular end-systolic volume(P<0. 05 and P<0. 01), and signifi-cantly increased the ejection fraction and the fractional shortening ( P <0. 01 ) . The histopathological changes of myocardium on myocardial infarction and fibrosis were dramatically reduced by TG. But ventricular wall was thicker. Two dose TG remarkably increased the expressions of VEGF and bFGF mRNA and micro ves-sel density of compositive CD31 + cells in ischemic myocardial tissue and around of infarct area(P<0. 01, P <0 . 0 5 ) . Conclusions TG could improve the car-diac function of acute myocardial infarction rat. The mechanism may be related to the upregulation of VEGF and bFGF gene expression, the promotion angiogene-sis, then the improvement of blood supply in myocardi-al infarction area.
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AIM:To investigate the myocardial protective effect of endometrial stem cell ( EnSC)-derived cyto-kine cocktail ( EdCC) on myocardial ischemic reperfusion injury and the MEK-ERK signaling pathway.METHODS: A mouse model of myocardial ischemic reperfusion injury was established.Infarct area, cell apoptosis, and expression of cleaved caspase-3 and phosphorylatied ERK1/2 were determined by TTC/Evans blue staining, TUNEL assay and Western blot, respectively.RESULTS:The mesenchymal characteristics were observed in the EnSCs with expressing CD90 and in absence of CD34 and CD45.EdCC contained (6 811 ±312) ng/g epidermal growth factor (EGF) protein.The phospho-rylation of ERK1/2 markedly increased after injection of EdCC, but was abolished by MEK1 inhibitor PD98059 ( 5 mg/kg) .EdCC decreased the infarct area and apoptotic cell number in the border zone and inhibited caspase-3 activation. However, the effects were abolished by MEK1 specific inhibitor PD98059.EGF did not decrease the infarct area, but the EGF receptor antagonist AG-1487 (6 mg/kg) partly abolished the myocardial protective effect of EdCC.CONCLUSION:EdCC protects the myocardium from ischemic reperfusion injury via activating MEK1-ERK signaling pathway, indicating an essential role in the transmission of stem cell therapy from the cell transplantation to cytokine based strategy.
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Acute myocardial infarction (AMI) model was made in SD rats by coronary ligation, the effects of naloxone (Nal) on the baroreflex sensitivity (BRS) were evaluated by administrated Nal intravenously (iv) and in-tracisternally (ic) before and after 1 h of AMI.Results showed that both pre and post AMI can Nal potentiate the BRS whether iv or ic. These results indicate that Nal may reverse the blunted BRS after AMI.