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Dexamethasone inhibits regeneration and causes ventricular aneurysm in the neonatal porcine heart after myocardial infarction.
Journal of Molecular and Cellular Cardiology ( IF 5 ) Pub Date : 2020-05-05 , DOI: 10.1016/j.yjmcc.2020.04.033
Zhonghao Tao 1 , Szejie Loo 2 , Liping Su 2 , Desiree Abdurrachim 3 , Janise Lalic 3 , Teck Hock Lee 3 , Xin Chen 4 , Ru-San Tan 2 , Jianyi Zhang 5 , Lei Ye 2
Affiliation  

AIMS Recently, we demonstrated that the hearts of neonatal pigs (2-day old) have regenerative capacity, likely driven by cardiac myocyte division, but this potential is lost immediately after postnatal day 3. However, it is unknown if corticosteroid, a broad anti-inflammatory agent, will abrogate the regenerative capacity in the hearts of neonatal pigs. The aim of the current study is to evaluate the effect Dexamethasone (Dex), a broad anti-inflammatory agent, on heart regeneration, structure, and function of the neonatal pigs' post-myocardial infarction (MI). METHODS AND RESULTS Dex (0.2 mg/kg/day) was injected intramuscularly into the neonatal pig (age: 2 days postnatal) during the first week post-MI. Myocardial scar and left ventricular function were determined by cardiac magnetic resonance (CMR) imaging. Bromodeoxyuridine (BrdU) pulse-chase labeling, histology, immunohistochemistry, and flow cytometry were performed to determine inflammatory cell infiltration, CM cytokinesis, and myocardial fibrosis. Dex injection during the first-week suppressed acute inflammation post-MI in the pig hearts. It inhibited BrdU incorporation to pig CMs and CM cytokinesis via inhibiting aurora-B protein expression which was associated with mature scar formation and thinned walls at the infarct site. CMR imaging showed Dex caused left ventricular aneurysm and poor ejection fraction. CONCLUSIONS Dex inhibited CM cytokinesis and functional recovery and caused ventricular aneurysm in the hearts of 2-day old pigs post-MI.

中文翻译:

地塞米松抑制心肌梗塞后新生猪心脏的再生并导致其室性动脉瘤。

AIMS最近,我们证明了新生猪(2天大)的心脏可能具有再生能力,这可能是由心肌细胞分裂驱动的,但是这种潜力在出生后第3天就立即消失了。 -炎症剂,将消除新生猪心脏的再生能力。本研究的目的是评估广泛的消炎药地塞米松(Dex)对新生猪心肌梗死(MI)的心脏再生,结构和功能的影响。方法和结果在心梗后的第一周内,将新生婴儿(年龄:产后2天)肌肉注射右旋糖酐(0.2 mg / kg /天)。心肌瘢痕和左心室功能通过心脏磁共振(CMR)成像确定。进行了溴脱氧尿苷(BrdU)脉冲追踪标记,组织学,免疫组织化学和流式细胞术的测定,以确定炎性细胞浸润,CM胞质分裂和心肌纤维化。在第一周内进行的右旋注射抑制了猪心脏MI后的急性炎症。它通过抑制与成熟疤痕形成和梗死部位壁变薄相关的极光B蛋白表达,抑制BrdU掺入猪CM和CM胞质分裂。CMR成像显示Dex引起左心室动脉瘤和射血分数差。结论Dex抑制了MI后2日龄猪心脏的CM胞质分裂和功能恢复,并引起了室性动脉瘤。和心肌纤维化。在第一周内进行的右旋注射抑制了猪心脏MI后的急性炎症。它通过抑制与成熟疤痕形成和梗死部位壁变薄相关的极光B蛋白表达,抑制BrdU掺入猪CM和CM胞质分裂。CMR成像显示Dex引起左心室动脉瘤和射血分数差。结论Dex抑制了MI后2日龄猪心脏的CM胞质分裂和功能恢复,并引起了室性动脉瘤。和心肌纤维化。在第一周内进行的右旋注射抑制了猪心脏MI后的急性炎症。它通过抑制与成熟疤痕形成和梗死部位壁变薄相关的极光B蛋白表达,抑制BrdU掺入猪CM和CM胞质分裂。CMR成像显示Dex引起左心室动脉瘤和射血分数差。结论Dex抑制了MI后2日龄猪心脏的CM胞质分裂和功能恢复,并引起了室性动脉瘤。CMR成像显示Dex引起左心室动脉瘤和射血分数差。结论Dex抑制了MI后2日龄猪心脏的CM胞质分裂和功能恢复,并引起了心室动脉瘤。CMR成像显示Dex引起左心室动脉瘤和射血分数差。结论Dex抑制了MI后2日龄猪心脏的CM胞质分裂和功能恢复,并引起了心室动脉瘤。
更新日期:2020-05-05
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