Human amniotic membrane mesenchymal stem cells exert cardioprotective effects against isoproterenol (ISO)-induced myocardial injury through suppression of inflammation and modulation of inflammatory MAPK/NF-κB pathway

被引:0
|
作者
Maryam Naseroleslami
Nahid Aboutaleb
机构
[1] Islamic Azad University,Department of Cellular and Molecular Biology, Faculty of Advanced Science and Technology, Tehran Medical Sciences
[2] Iran University of Medical Sciences,Physiology Research Center
[3] Iran University of Medical Sciences,Department of Physiology, Faculty of Medicine
来源
Cell and Tissue Banking | 2022年 / 23卷
关键词
Mesenchymal stem cells; Isoproterenol (ISO)-induced myocardial injury; MAPK; NF-κB pathway; Inflammation;
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学科分类号
摘要
A common cause of mortality around the world is ischemic myocardial injury. The study was conducted to examine the ability of amniotic membrane mesenchymal stem cells (AMSCs) for protection against isoproterenol (ISO)-induced myocardial injury and attempted to show the possible mechanisms by which AMSCs that can be linked to inhibition of inflammation by targeting inflammatory MAPK/NF-κB pathway. Model was established by subcutaneous injection of 170 mg/kg/day of ISO for four consecutive days. Flow cytometry and echocardiography were carried out to evaluate characterization of hAMSCs and cardiac function, respectively. The expression of inflammatory cytokines was determined using ELISA assay. The activities of NF-κB and phosphorylated p38 MAPK were measured using immunohistochemical assessments. The results showed that ISO administration was resulted in cardiac dysfunction, increased levels of inflammatory cytokines that reversed by intramyocardially administration of AMSCs (P < 0. 05). Cardioprotective effects of AMSCs were associated with a significant decreased expression of NF-κB and reduced levels of phosphorylated p38 MAPK (P < 0. 05). In conclusion, our finding showed that intramyocardially administration of AMSCs could contribute to improvement of heart function and inhibition of inflammation in the site of injury by targeting inflammatory MAPK/NF-κB pathway.
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页码:67 / 77
页数:10
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