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人羊膜间充质干细胞条件培养基通过靶向氧化应激减轻大鼠心肌缺血再灌注损伤。

Human amniotic membrane mesenchymal stem cells-conditioned medium attenuates myocardial ischemia-reperfusion injury in rats by targeting oxidative stress.

作者信息

Mokhtari Behnaz, Azizi Yaser, Rostami Abookheili Aliakbar, Aboutaleb Nahid, Nazarinia Donya, Naderi Nasim

机构信息

Physiology Research Center, Iran University of Medical Sciences, Tehran, Iran.

Department of Physiology, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran.

出版信息

Iran J Basic Med Sci. 2020 Nov;23(11):1453-1461. doi: 10.22038/ijbms.2020.47572.10952.

DOI:10.22038/ijbms.2020.47572.10952
PMID:33235703
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7671430/
Abstract

OBJECTIVES

Ischemic heart diseases (IHD) are one of the major causes of death worldwide. Studies have shown that mesenchymal stem cells can secrete and release conditioned medium (CM) which has biological activities and can repair tissue injury. This study aimed to investigate the effects of human amniotic membrane mesenchymal stem cells (hAMCs)-CM on myocardial ischemia/reperfusion (I/R) injury in rats by targeting oxidative stress.

MATERIALS AND METHODS

Male Wistar rats (40 rats, weighing 200-250 g) were randomly divided into four groups: Sham, myocardial infarction (MI), MI + culture media, and MI + conditioned medium. MI was induced by ligation of the left anterior descending coronary artery for 30 min. After 15 min of reperfusion, intramyocardial injections of hAMCs-CM or culture media (150 μl) were performed. At the end of the experiment, serum levels of cardiac troponin-I (cTn-I), myocardial levels of malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GPx), as well as cardiac histological changes were evaluated.

RESULTS

HAMCs-CM significantly decreased cTn-I and MDA levels and increased SOD and GPx activities (<0.05). In addition, hAMCs-CM improved cardiac histological changes and decreased myocardial injury percentage (<0.05).

CONCLUSION

This study showed that hAMCs-CM has cardioprotective effects in the I/R injury condition. Reduction of oxidative stress by hAMCs-CM plays a significant role in this context. Based on the results of this study, it can be concluded that hAMCs-CM can be offered as a therapeutic candidate for I/R injury in the future, but more research is needed.

摘要

目的

缺血性心脏病(IHD)是全球主要的死亡原因之一。研究表明,间充质干细胞可分泌并释放具有生物活性且能修复组织损伤的条件培养基(CM)。本研究旨在通过靶向氧化应激来探讨人羊膜间充质干细胞(hAMCs)-CM对大鼠心肌缺血/再灌注(I/R)损伤的影响。

材料与方法

雄性Wistar大鼠(40只,体重200 - 250 g)随机分为四组:假手术组、心肌梗死(MI)组、MI + 培养基组和MI + 条件培养基组。通过结扎左冠状动脉前降支30分钟诱导MI。再灌注15分钟后,进行心肌内注射hAMCs-CM或培养基(150 μl)。实验结束时,评估血清心肌肌钙蛋白I(cTn-I)水平、心肌丙二醛(MDA)、超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GPx)水平以及心脏组织学变化。

结果

hAMCs-CM显著降低cTn-I和MDA水平,并增加SOD和GPx活性(<0.05)。此外,hAMCs-CM改善了心脏组织学变化并降低了心肌损伤百分比(<0.05)。

结论

本研究表明hAMCs-CM在I/R损伤情况下具有心脏保护作用。hAMCs-CM减轻氧化应激在这一过程中起重要作用。基于本研究结果,可以得出结论:hAMCs-CM未来可作为I/R损伤的治疗候选物,但还需要更多研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16eb/7671430/26cefd2b2248/IJBMS-23-1453-g006.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16eb/7671430/f45cd9184062/IJBMS-23-1453-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16eb/7671430/26cefd2b2248/IJBMS-23-1453-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16eb/7671430/0e575f63d46f/IJBMS-23-1453-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16eb/7671430/bcfe32456f62/IJBMS-23-1453-g002.jpg
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