Suppr超能文献

(沃尔.)梅斯嫩。醇提物减轻内皮细胞激活并缓解心肌缺血再灌注损伤。

(Wall.) Meisn. Ethanolic Extract Attenuates Endothelial Activation and Alleviates Cardiac Ischemia-Reperfusion Injury.

机构信息

Center for Translational Medicine, Jiangxi University of Chinese Medicine, Nanchang 330004, China.

Department of Cardiovascular Sciences, Center for Metabolic Disease Research, Lewis Katz School of Medicine, Temple University, Philadelphia, PA 19140, USA.

出版信息

Molecules. 2024 Feb 29;29(5):1068. doi: 10.3390/molecules29051068.

Abstract

Endothelial pro-inflammatory activation is pivotal in cardiac ischemia-reperfusion (I/R) injury pathophysiology. The dried flower bud of (Wall.) Meisn. (EG) is a commonly utilized traditional Tibetan medicine. However, its role in regulating endothelium activation and cardiac I/R injury has not been investigated. Herein, we showed that the administration of EG ethanolic extract exhibited a potent therapeutic efficacy in ameliorating cardiac endothelial inflammation ( < 0.05) and thereby protecting against myocardial I/R injury in rats ( < 0.001). In line with the in vivo findings, the EG extract suppressed endothelial pro-inflammatory activation in vitro by downregulating the expression of pro-inflammatory mediators ( < 0.05) and diminishing monocytes' firm adhesion to endothelial cells (ECs) ( < 0.01). Mechanistically, we showed that EG extract inhibited the nuclear factor kappa-B (NF-κB), c-Jun -terminal kinase (JNK), extracellular regulated protein kinase (ERK), and p38 mitogen-activated protein kinase (MAPK) signaling pathways to attenuate EC-mediated inflammation ( < 0.05). Collectively, for the first time, this study demonstrated the therapeutic potential of EG ethanolic extract in alleviating I/R-induced inflammation and the resulting cardiac injury through its inhibitory role in regulating endothelium activation.

摘要

内皮细胞促炎激活在心肌缺血再灌注(I/R)损伤发病机制中起着关键作用。(Wall.)Meisn. 的干花蕾(EG)是一种常用的传统藏药。然而,其在调节内皮细胞激活和心肌 I/R 损伤中的作用尚未得到研究。本文表明,EG 乙醇提取物的给药在改善心脏内皮炎症方面表现出强大的治疗功效(<0.05),从而保护大鼠免受心肌 I/R 损伤(<0.001)。与体内发现一致,EG 提取物通过下调促炎介质的表达(<0.05)和减少单核细胞与内皮细胞(ECs)的牢固黏附(<0.01)来抑制体外内皮促炎激活。从机制上讲,我们表明 EG 提取物抑制核因子 kappa-B(NF-κB)、c-Jun 末端激酶(JNK)、细胞外调节蛋白激酶(ERK)和 p38 丝裂原活化蛋白激酶(MAPK)信号通路,从而减轻 EC 介导的炎症(<0.05)。总之,这项研究首次表明,EG 乙醇提取物通过抑制内皮细胞激活来调节内皮细胞激活,从而在缓解 I/R 诱导的炎症和由此产生的心肌损伤方面具有治疗潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a9e/10935089/bdefe9488677/molecules-29-01068-g001.jpg

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验