The difficulty in the regeneration of cardiomyocytes after myocardial infarction is a major cause of heart failure. Together, the amniotic membrane and 15-deoxy-Δ12,14-prostaglandin J2 (15d-PGJ₂) can help in the recovery of cardiomyocyte, as they present many growth factors and anti-inflammatory effect, respectively. The objective of this study is to compare the efficacy of Human Decellularized Amniotic Membrane Scaffold (AHAS) loaded with 15d-PGJ₂ in improving ventricular function in a rat model of postinfarct ventricular dysfunction. Myocardial infarction was induced in 24 rats by left coronary occlusion. After a week, the animals were subjected to echocardiography for evaluation of left ventricle ejection fraction (LVEF), left ventricle end diastolic volume (LVEDV), and left ventricle end systolic volume (LVESV). Animals with ejection fraction <40% were included in the study and were randomized into three groups: control (n = 8), AHAS (n = 8) and AHAS +15d-PGJ₂ (n = 8). In the AHAS group only the membrane was implanted, whereas in the AHAS +15d-PGJ₂ the membrane +15d-PGJ₂ was implanted on myocardial infarction. Echocardiographic evaluation was performed after 1 month. For histological analysis, heart tissue was stained with Gomori trichome, Sirius Red, the antibody against CD31 and connexin 43 (Cx43). There were no significant differences in the baseline LVEF, LVEDV, and LVESV in all groups. After 1 month, ejection fraction decreased in the control group but increased in the AHAS group and in the AHAS +15d-PGJ₂ group in comparison with the control group. The LVEDV and LVESV in the AHAS and AHAS +15d-PGJ₂ groups decreased compared with the control group, featuring a ventricular antiremodeling effect. Histopathology of the infarcted area identified the reduction of infarct size and collagen type 1 in the AHAS and AHAS +15d-PGJ₂ groups. New blood vessels and cardiomyocytes have been identified in an infarcted area by CD31 and Cx43. AHAS +15d-PGJ₂ provided an increase in the ejection fraction and prevented ventricular dilation in this postinfarction ventricular dysfunction model.

中文翻译：

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在梗塞后大鼠模型中具有 15d-PGJ2 纳米颗粒的脱细胞人羊膜支架。

心肌梗塞后心肌细胞再生困难是导致心力衰竭的主要原因。羊膜和 15-脱氧-Δ12,14-前列腺素 J2 (15d-PGJ ₂ ) 一起可以帮助心肌细胞的恢复，因为它们分别具有许多生长因子和抗炎作用。本研究的目的是比较载有 15d-PGJ ₂的人脱细胞羊膜支架 (AHAS) 的功效在改善梗塞后心室功能障碍大鼠模型中的心室功能。24只大鼠因左冠状动脉闭塞诱发心肌梗塞。一周后，对动物进行超声心动图以评估左心室射血分数 (LVEF)、左心室舒张末期容积 (LVEDV) 和左心室收缩末期容积 (LVESV)。射血分数 <40% 的动物被纳入研究并随机分为三组：对照组 ( n  = 8)、AHAS ( n  = 8) 和 AHAS +15d-PGJ ₂ ( n  = 8)。在 AHAS 组中仅植入了膜，而在 AHAS +15d-PGJ _{2 中}植入了膜 +15d-PGJ ₂植入心肌梗塞。1个月后进行超声心动图评估。对于组织学分析，心脏组织用 Gomori 毛状体、天狼星红、CD31 和连接蛋白 43 (Cx43) 的抗体染色。所有组的基线 LVEF、LVEDV 和 LVESV 均无显着差异。1个月后，与对照组相比，对照组的射血分数下降，但AHAS组和AHAS+15d-PGJ ₂组的射血分数增加。AHAS和AHAS+15d-PGJ ₂组的LVEDV和LVESV较对照组降低，具有心室抗重构作用。梗死区域的组织病理学确定了 AHAS 和 AHAS +15d-PGJ ₂中梗死面积和 1 型胶原蛋白的减少组。CD31 和 Cx43 已在梗塞区域识别出新的血管和心肌细胞。在这个梗塞后心室功能障碍模型中，AHAS +15d-PGJ ₂增加了射血分数并防止了心室扩张。