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Effect of Irisin on Pressure Overload-Induced Cardiac Remodeling.

Irisin对压力超负荷诱导的心脏重构的影响。

  • 影响因子:2.10
  • DOI:10.1016/j.arcmed.2020.10.006
  • 作者列表:"Peng Q","Ding R","Wang X","Yang P","Jiang F","Chen X
  • 发表时间:2021-02-01
Abstract

BACKGROUND:Irisin has been considered a prognostic factor in several cardiovascular diseases. Nevertheless, no data are available on the role of irisin in cardiac remodeling. AIM OF THE STUDY:This study aimed to determine the potential role of irisin in cardiac remodeling and explore potential mechanisms. METHODS:A total of 40 rats that underwent transverse abdominal aortic constriction (TAC) surgery or sham operation were divided into four groups: sham + saline (NS), sham + irisin, TAC + NS, and TAC + irisin. After 6 weeks of treatment, echocardiography was performed to assess in vivo cardiac morphology. The left ventricular myocardium was prepared and observed by pathological examination. The effect of irisin on cardiomyocyte apoptosis and the expression of oxidative stress and cardiac hypertrophy markers were observed. Then, the effect of irisin on the Akt signaling system was also detected. RESULTS:The rats in the TAC group displayed obvious signs of cardiac dysfunction and cardiac hypertrophy, and irisin treatment could reverse these changes. Irisin could inhibit the expression of nicotinamide adenine dinucleotide phosphate oxidase 2 and xanthine oxidase in TAC rats and increase the expression of antioxidant enzymes. Furthermore, the expression of phosphorylated protein kinase B (p-Akt), phosphorylated mammalian target of rapamycin (p-mTOR), and phosphorylated glycogen synthase kinase 3β (p-GSK3β) was much higher in the cardiac remodeling groups (p <0.05 vs. sham rats). Irisin could relieve the inhibition effect and reduce the expression level of these three proteins. CONCLUSIONS:Irisin treatment could significantly improve cardiac remodeling by inhibiting oxidative stress via attenuating the Akt signaling activation.

摘要

背景: Irisin被认为是多种心血管疾病的预后因素。然而,没有关于irisin在心脏重塑中的作用的数据。 研究目的: 本研究旨在确定irisin在心脏重塑中的潜在作用并探讨潜在机制。 方法: 40只接受腹主动脉缩窄术 (TAC) 或假手术的大鼠分为4组: 假手术 + 生理盐水 (NS) 、假手术 + irisin、TAC + NS和TAC + irisin。治疗6周后,进行超声心动图以评估体内心脏形态。制备左心室心肌,并进行病理观察。观察irisin对心肌细胞凋亡及氧化应激和心肌肥厚标志物表达的影响。然后,还检测了irisin对Akt信号系统的影响。 结果: TAC组大鼠出现明显的心功能障碍和心肌肥厚征象,irisin治疗可逆转这些变化。Irisin可抑制TAC大鼠烟酰胺腺嘌呤二核苷酸磷酸氧化酶2和黄嘌呤氧化酶的表达,增加抗氧化酶的表达。此外,心脏重塑组中磷酸化蛋白激酶B (p-Akt) 、磷酸化哺乳动物雷帕霉素靶蛋白 (p-mTOR) 和磷酸化糖原合成酶激酶3β (p-GSK3β) 的表达明显高于假手术组 (p <0.05)。Irisin可以减轻抑制作用并降低这三种蛋白的表达水平。 结论: Irisin治疗可通过抑制Akt信号活化抑制氧化应激而显著改善心脏重构。

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发表时间:2021-02-01
DOI:10.1080/14656566.2020.1814255
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DOI:10.1007/s11033-021-06299-9
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