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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >N-acetyl-seryl-aspartyl-lysyl-proline treatment protects heart against excessive myocardial injury and heart failure in mice
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N-acetyl-seryl-aspartyl-lysyl-proline treatment protects heart against excessive myocardial injury and heart failure in mice

机译：N-乙酰基 - 阿氨酰 - 溶脯氨酸治疗保护心脏免受小鼠的过度心肌损伤和心力衰竭

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摘要

Myocardial infarction (MI) in mice results in cardiac rupture at 4-7 days after MI, whereas cardiac fibrosis and dysfunction occur later. N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) has anti-inflammatory, anti-fibrotic, and pro-angiogenic properties. We hypothesized that Ac-SDKP reduces cardiac rupture and adverse cardiac remodeling, and improves function by promoting angiogenesis and inhibiting detrimental reactive fibrosis and inflammation after MI. C57BL/6J mice were subjected to MI and treated with Ac-SDKP (1.6 mg/kg per day) for 1 or 5 weeks. We analyzed (1) intercellular adhesion molecule-1 (ICAM-1) expression; (2) inflammatory cell infiltration and angiogenesis; (3) gelatinolytic activity; (4) incidence of cardiac rupture; (5) p53, the endoplasmic reticulum stress marker CCAAT/enhancer binding protein homology protein (CHOP), and cardiomyocyte apoptosis; (6) sarcoplasmic reticulum Ca2+ ATPase (SERCA2) expression; (7) interstitial collagen fraction and capillary density; and (8) cardiac remodeling and function. Acutely, Ac-SDKP reduced cardiac rupture, decreased ICAM-1 expression and the number of infiltrating macrophages, decreased gelatinolytic activity, p53 expression, and myocyte apoptosis, but increased capillary density in the infarction border. Chronically, Ac-SDKP improved cardiac structures and function, reduced CHOP expression and interstitial collagen fraction, and preserved myocardium SERCA2 expression. Thus, Ac-SDKP decreased cardiac rupture, ameliorated adverse cardiac remodeling, and improved cardiac function after MI, likely through preserved SERCA2 expression and inhibition of endoplasmic reticulum stress.
机译：小鼠中的心肌梗死（MI）导致MI后4-7天的心脏破裂，而心肌纤维化和功能障碍发生在后期。 N-乙酰 - 甲基 - α-丙氨酸 - 赖氨酸（AC-SDKP）具有抗炎，抗纤维化和促血管生成性能。我们假设AC-SDKP降低心脏破裂和不良心脏重塑，并通过促进血管生成和抑制MI后的有害活性纤维化和炎症来改善功能。将C57BL / 6J小鼠进行MI，并用AC-SDKP（每天1.6mg / kg）处理1或5周。我们分析（1）细胞间粘附分子-1（ICAM-1）表达; （2）炎症细胞浸润和血管生成; （3）凝胶溶解度; （4）心脏破裂的发病率; （5）P53，内质网应激标记物CCAAT / Enhancer结合蛋白质同源蛋白（Chec）和心肌细胞凋亡; （6）肌肉网+ ATP酶（SERCA2）表达; （7）间质胶原胶原馏分和毛细血管密度; （8）心脏重塑和功能。急性，AC-SDKP减少心脏破裂，降低ICAM-1表达和渗透巨噬细胞的数量，降低凝胶溶解活性，P53表达和肌细胞凋亡，但梗死边界中的毛细密度增加。慢性病，AC-SDKP改善了心脏结构和功能，减少了切碎的表达和间质胶原蛋白分数，并保存了心肌Serca2表达。因此，AC-SDKP减少了心脏破裂，改善的不良心脏重塑，并且在MI后改善的心脏功能，可能通过保存的SERCA2表达和内质网应力的抑制。

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