Medical Journal of The Islamic Republic of Iran (MJIRI)

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  Abstract

  Background: Recently, small dense low density lipoprotein (sdLDL) has been

  highlighted as a new risk factor for the coronary artery disease (CAD).Small dense

  LDLs are believed to be atherogenic since these particles are taken up more easily by

  arterial wall. They are readily oxidized and have reduced affinity for low density

  lipoprotein (LDL) receptor and increased affinity for arterial proteoglicans. LDL

  cholesterol is only a measure of the cholesterol level in the LDL whereas apolipoprotein

  B(apo B) is a measure of the cholesterol levels of all the atherogenic particles, including

  very low density lipoprotein, intermediate density, and low density lipoproteins.

  Therefore, it might be a better marker than other traditional lipids. The aim of

  the present study was to evaluate the association between serum small dense LDL,

  apolipoprotein B, apolipoprotein A1 (apo A1) and apoB/apoA1 ratio and the coronary

  stenosis.

  Methods: 86 patients with coronary stenosis , 35 patients without coronary stenosis

  identified by angiography who were referred to Rajaii Heart Center , and 30

  healthy individuals were studied. SdLDL was measured by a direct homogenous

  LDL-C assay in the supernatant of serum which remained after heparin-magnesium

  precipitation. Serum apolipoprotein A1 and apolipoprotein B were measured by using

  immunoturbidimetric method.

  Results: The results showed that the sdLDL levels were higher in patients with

  coronary stenosis than patients without coronary stenosis and healthy individuals

  (21.54±7.1, 16.88±4.4 and 15.45±5mg/dl, p=0.001, respectively). In addition the level

  of apoB (with stenosis: 113.71±21.8, without stenosis:100.88±18.7 and healthy:

  102.30±9.6, p=0.003) and apoB/apoA1 ratio (with stenosis:1.100±0.24, without

  stenosis :0.589±0.26 and healthy:0.751±0.16, p=0.001) were significantly higher in

  patients with coronary stenosis. SdLDL levels were positively correlated with the

  level of apoB(r=0.589), apoB/apoA1 ratio(r=0.416), triglyceride(r=0.494), LDL-C

  (r=0.749), Total cholesterol(r=0.354) and were inversely correlated with the level of

  HDL-C (r = -0.586)(p<0.01).

  Conclusion: The elevated levels of small dense LDL, apoB and apoB/apoA1 ratio

  were associated with coronary artery stenosis.

 

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Background: Ischemic cardiomyopathies are the leading causes of mortality and morbidity. Stem cell therapy using amniotic membrane mesenchymal stem cells have emerged as a promising cardiac regeneration modality. They have shown great immunological advantage when used in allogeneic or xenogeneic transplantation. The aim of the current study is to accumulate evidence from published preclinical studies on the application of amniotic membrane derived mesenchymal stem cells (AMSCs) in the treatment of ischemic cardiomyopathies including myocardial ischemia and heart failure. The aim is to define if there is enough high-quality current evidence to support starting the use of these cells in clinical trials.
   Methods: PubMed, SCOPUS, EMBASE, and ISI Web of Science databases were searched without temporal and language restrictions. Data were extracted from selected studies. The primary outcomes were left ventricular ejection fraction (LVEF) and LV fibrosis. The risk of bias (ROB) assessment was performed using SYRCLE’s ROB tool. After qualitative synthesis, provided that data meets the criteria for quantitative analysis, a meta-analysis was performed using Stata software V12 to investigate the heterogeneity of the data and to get an overall estimate of the effect size of the treatment on each outcome.
   Results: On primary search, 438 citations were retrieved. After screening, three studies were selected for quantitative analysis of each of the outcomes LVEF and LV fibrosis. Their administration in acute and chronic MI alleviates heart failure and improves LVEF (SMD=3.56, 95% CI: 2.24-4.87, I-squared=83.1%, p=0.003) and reduces infarct size (SMD= -4.41, 95% CI: (-5.68)-(-3.14), I-squared=79.0%, p=0.009). These observations were achieved in the acute MI model, HF following ischemia due to coronary artery stenosis and coronary artery occlusion with the early restoration of the perfusion.
   Conclusion: Present low and medium quality evidence from preclinical studies confirm the efficacy of the AMSCs in the preclinical models of acute MI and HF following ischemia due to coronary artery stenosis and permanent/temporary coronary artery occlusion. High-quality preclinical studies are indicated to bridge the gaps in translation of the current findings of AMSCs research for the treatment of patients with acute and chronic myocardial ischemia and heart failure.

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    Background: Currently, stem cell therapy has been proposed as an efficient strategy to prevent or treat myocardial injuries. The current study was conducted to examine cardioprotective effects of human mesenchymal stem cells derived from amniotic membrane (hAMSCs) against isoproterenol (ISO)-induced myocardial injury and explore its potential mechanisms.
    Methods: The hAMSCs were injected intramyocardially in male Wistar rats 28 days after last injection of ISO (170 mg/kg body weight for 4 consecutive days). The echocardiography was performed to confirm induction of myocardial damage and cardiac function 28 days after last injection of ISO and 4 weeks hAMSCs transplantation after HF induction. The expression of apoptotic markers such as Bcl-2, Bax and P53 was evaluated using Western blotting assay. Masson’s trichrome staining was used to determine fibrosis. The cytoarchitecture of myocardial wall and morphology of cells were investigated using hematoxylin and eosin (H&E) staining.
   Results: As compared to ISO group, hAMSCs transplantation after heart failure (HF) induction significantly blunted the increasing of cardiac dimensions and restored ejection fraction (EF) and fractional shortening (FS) parameters (p<0.05). Moreover, hAMSCs transplantation after HF induction increased the expression of antiapoptotic markers such as Bcl-2 and decreased the expression of pro-apoptotic markers such as P53 and Bax (p<0.05). As compared to ISO group, hAMSCs transplantation after HF induction markedly reduced interstitial myocardial fibrosis and contributed to maintain of normal cytoarchitecture of myocardial wall and morphology of cells.
   Conclusion: Collectively, the results of current study suggest that transplantation of hAMSCs confers cardioprotection by targeting ISO‐induced mitochondria‐dependent (intrinsic) pathway of apoptosis.