Suppr超能文献

霍诺酚醇通过激活自噬保护抗 1 肾上腺素能受体自身抗体诱导的心肌功能障碍。

Honokiol Protects against Anti-1-Adrenergic Receptor Autoantibody-Induced Myocardial Dysfunction via Activation of Autophagy.

机构信息

Department of Cardiology, Affiliated Hospital of Jining Medical University, Jining, Shandong 272129, China.

Department of Cardiology, Yantai Yuhuangding Hospital, Affiliated Hospital of Qingdao University, Yantai, Shandong 264000, China.

出版信息

Oxid Med Cell Longev. 2018 Jul 18;2018:1640804. doi: 10.1155/2018/1640804. eCollection 2018.

Abstract

Myocardial diseases are prevalent syndromes with high mortality rate. The exploration of effective interference is important. Anti-1-adrenergic receptor autoantibody (1-AAB) is highly correlated with myocardial dysfunction. The actions and underlying mechanisms of honokiol (HNK) in 1-AAB-positive patients await to be unraveled. In this study, we established a rat model of 1-AAB positive with myocardial dysfunction. Cardiac function following 1-AR-ECII administration was analyzed using the VisualSonics Vevo 770 High-Resolution In Vivo Imaging System. The levels of autophagy-related proteins were detected by Western blotting. Our data revealed that HNK reversed 1-AAB-induced effects and protected myocardial tissues from dysfunction. After HNK treatment, the cardiac contractile ability increased and the LDH activity decreased. HNK attenuated myocardial degeneration. In addition, HNK promoted the activation of the AMP-dependent protein kinase/Unc-51-like autophagy activating kinase (AMPK/ULK) pathway and activated autophagy. These results suggest that HNK protects against 1-AAB-induced myocardial dysfunction via activation of autophagy and it may be a potentially therapeutic compound for 1-AAB-positive myocardial diseases.

摘要

心肌疾病是一种常见的综合征,死亡率很高。探索有效的干预措施非常重要。抗 1 肾上腺素能受体自身抗体(1-AAB)与心肌功能障碍高度相关。霍诺醇(HNK)在 1-AAB 阳性患者中的作用和潜在机制有待阐明。在这项研究中,我们建立了一种伴有心肌功能障碍的 1-AAB 阳性大鼠模型。使用 VisualSonics Vevo 770 高分辨率体内成像系统分析 1-AR-ECII 给药后的心脏功能。通过 Western blot 检测自噬相关蛋白的水平。我们的数据显示,HNK 逆转了 1-AAB 诱导的作用,保护心肌组织免受功能障碍。HNK 治疗后,心脏收缩能力增加,LDH 活性降低。HNK 减轻了心肌变性。此外,HNK 促进了 AMP 依赖的蛋白激酶/Unc-51 样自噬激活激酶(AMPK/ULK)途径的激活,并激活了自噬。这些结果表明,HNK 通过激活自噬来保护 1-AAB 诱导的心肌功能障碍,它可能是一种治疗 1-AAB 阳性心肌疾病的潜在治疗化合物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16af/6079338/19e665d05b41/OMCL2018-1640804.001.jpg

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验