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葡萄籽原花青素提取物通过PI3K/AKT通路改善小鼠心肌梗死后的心脏重塑

Grape Seed Proanthocyanidin Extract Ameliorates Cardiac Remodelling After Myocardial Infarction Through PI3K/AKT Pathway in Mice.

作者信息

Ruan Yongxue, Jin Qike, Zeng Jingjing, Ren Fangfang, Xie Zuoyi, Ji Kangting, Wu Lianpin, Wu Jingguo, Li Lei

机构信息

Department of Cardiology, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China.

Department of General Internal Medicine, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.

出版信息

Front Pharmacol. 2020 Dec 4;11:585984. doi: 10.3389/fphar.2020.585984. eCollection 2020.

Abstract

Myocardial infarction is one of the most serious fatal diseases in the world, which is due to acute occlusion of coronary arteries. Grape seed proanthocyanidin extract (GSPE) is an active compound extracted from grape seeds that has anti-oxidative, anti-inflammatory and anti-tumor pharmacological effects. Natural products are cheap, easy to obtain, widely used and effective. It has been used to treat numerous diseases, such as cancer, brain injury and diabetes complications. However, there are limited studies on its role and associated mechanisms in myocardial infarction in mice. This study showed that GSPE treatment in mice significantly reduced cardiac dysfunction and improved the pathological changes due to MI injury. , GSPE inhibited the apoptosis of H9C2 cells after hypoxia culture, resulting in the expression of Bax decreased and the expression of Bcl-2 increased. The high expression of p-PI3K and p-AKT was detected in MI model and . The use of the specific PI3K/AKT pathway inhibitor LY294002 regressed the cardio-protection of GSPE. Our results showed that GSPE could improve the cardiac dysfunction and remodeling induced by MI and inhibit cardiomyocytes apoptosis in hypoxic conditions through the PI3K/AKT signaling pathway.

摘要

心肌梗死是世界上最严重的致命疾病之一,它是由冠状动脉急性闭塞引起的。葡萄籽原花青素提取物(GSPE)是一种从葡萄籽中提取的活性化合物,具有抗氧化、抗炎和抗肿瘤药理作用。天然产物价格便宜、易于获取、广泛使用且有效。它已被用于治疗多种疾病,如癌症、脑损伤和糖尿病并发症。然而,关于其在小鼠心肌梗死中的作用及相关机制的研究有限。本研究表明,对小鼠进行GSPE治疗可显著减轻心脏功能障碍,并改善心肌梗死损伤所致的病理变化。GSPE抑制了缺氧培养后H9C2细胞的凋亡,导致Bax表达降低,Bcl-2表达增加。在心肌梗死模型中检测到p-PI3K和p-AKT的高表达。使用特异性PI3K/AKT途径抑制剂LY294002可使GSPE的心脏保护作用消退。我们的结果表明,GSPE可改善心肌梗死所致的心脏功能障碍和重塑,并通过PI3K/AKT信号通路抑制缺氧条件下心肌细胞的凋亡。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f1dd/7747856/27dc78a44816/fphar-11-585984-g001.jpg

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