Suppr超能文献

异鼠李素通过阻断PI3K-AKT信号通路预防心肌肥大。

Isorhamnetin protects against cardiac hypertrophy through blocking PI3K-AKT pathway.

作者信息

Gao Lu, Yao Rui, Liu Yuzhou, Wang Zheng, Huang Zhen, Du Binbin, Zhang Dianhong, Wu Leiming, Xiao Lili, Zhang Yanzhou

机构信息

Department of Cardiology, The First Affiliated Hospital of Zhengzhou University, No.1 Jianshe East Road, Zhengzhou, 450052, China.

出版信息

Mol Cell Biochem. 2017 May;429(1-2):167-177. doi: 10.1007/s11010-017-2944-x. Epub 2017 Feb 7.

Abstract

Isorhamnetin, a flavonoid compound extracted from the Chinese herb Hippophae rhamnoides L., is well known for its anti-inflammatory, anti-oxidative, anti-adipogenic, anti-proliferative, and anti-tumor activities. However, the role of isorhamnetin in cardiac hypertrophy has not been reported. The aims of the present study were to find whether isorhamnetin could alleviate cardiac hypertrophy and to define the underlying molecular mechanisms. Here, we investigated the effects of isorhamnetin (100 mg/kg/day) on cardiac hypertrophy induced by aortic banding in mice. Cardiac hypertrophy was evaluated by echocardiographic, hemodynamic, pathological, and molecular analyses. Our data demonstrated that isorhamnetin could inhibit cardiac hypertrophy and fibrosis 8 weeks after aortic banding. The results further revealed that the effect of isorhamnetin on cardiac hypertrophy was mediated by blocking the activation of phosphatidylinositol 3-kinase-AKT signaling pathway. In vitro studies performed in neonatal rat cardiomyocytes confirmed that isorhamnetin could attenuate cardiomyocyte hypertrophy induced by angiotensin II, which was associated with phosphatidylinositol 3-kinase-AKT signaling pathway. In conclusion, these data indicate for the first time that isorhamnetin has protective potential for targeting cardiac hypertrophy by blocking the phosphatidylinositol 3-kinase-AKT signaling pathway. Thus, our study suggests that isorhamnetin may represent a potential therapeutic strategy for the treatment of cardiac hypertrophy and heart failure.

摘要

异鼠李素是一种从中国草药沙棘中提取的黄酮类化合物,因其抗炎、抗氧化、抗脂肪生成、抗增殖和抗肿瘤活性而闻名。然而,异鼠李素在心脏肥大中的作用尚未见报道。本研究的目的是探究异鼠李素是否能减轻心脏肥大,并确定其潜在的分子机制。在此,我们研究了异鼠李素(100毫克/千克/天)对小鼠主动脉缩窄诱导的心脏肥大的影响。通过超声心动图、血流动力学、病理学和分子分析来评估心脏肥大。我们的数据表明,异鼠李素可在主动脉缩窄8周后抑制心脏肥大和纤维化。结果进一步显示,异鼠李素对心脏肥大的作用是通过阻断磷脂酰肌醇3激酶-AKT信号通路的激活来介导的。在新生大鼠心肌细胞中进行的体外研究证实,异鼠李素可减轻血管紧张素II诱导的心肌细胞肥大,这与磷脂酰肌醇3激酶-AKT信号通路有关。总之,这些数据首次表明,异鼠李素通过阻断磷脂酰肌醇3激酶-AKT信号通路对心脏肥大具有保护潜力。因此,我们的研究表明,异鼠李素可能是治疗心脏肥大和心力衰竭的一种潜在治疗策略。

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