木犀草素抑制前列腺素内过氧化物合酶2缓解动静脉瘘新生内膜增生的作用。

IF 3.2 3区 生物学 Q3 MATERIALS SCIENCE, BIOMATERIALS
Ruibin Zhang, Wei Li, Jihua Yang, Xiujie Fan, Huili Fan, Wei Li
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引用次数: 0

摘要

本研究旨在探讨木犀草素在动静脉瘘(AVF)模型血管平滑肌细胞(VSMCs)炎症和表型转换中的作用及机制,为预防和治疗AVF新生内膜增生提供可能的药物。在体内,建立了Sprague Dawley大鼠AVF模型。在体外,用血小板衍生生长因子- bb (PDGF-BB)处理大鼠VSMCs,诱导VSMCs表型转换。用苏木精-伊红分析组织学AVF变化。采用Western blot和定量实时聚合酶链反应(qRT-PCR)检测前列腺素内过氧化物合成酶2 (PTGS2)的表达。在体内,木犀草素抑制新内膜的形成,降低vimentin、α-SMA、MCP-1、MMP-9、TNF-α和IL-6水平。在体外,PDGF-BB处理下,木犀草素抑制VSMCs的增殖和迁移,降低TNF-α、vimentin、α-SMA、MCP-1、MMP-9和IL-6水平。在大鼠AVF组织中,PTGS2表达升高。木犀草素在体内和体外抑制PTGS2的表达。PTGS2过表达逆转木草素在PDGF-BB治疗的vsmc细胞外基质蛋白表达、增殖、炎症和迁移中的作用。总之,在AVF中,木樨草素通过抑制PTGS2表达抑制VSMCs的增殖、迁移、表型转换、新内膜形成和炎症反应。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

The Role of Luteolin in Inhibiting Prostaglandin-Endoperoxide Synthase 2 to Relieve Neointimal Hyperplasia in Arteriovenous Fistula

The Role of Luteolin in Inhibiting Prostaglandin-Endoperoxide Synthase 2 to Relieve Neointimal Hyperplasia in Arteriovenous Fistula

This study aims to investigate the role and mechanism of luteolin in inflammation and phenotypic switch of vascular smooth muscle cells (VSMCs) in an arteriovenous fistula (AVF) model, for providing a potential agent for the prevention and therapy of AVF neointimal hyperplasia. In vivo, an AVF model is created in Sprague Dawley rats. In vitro, rat VSMCs are treated with platelet-derived growth factor-BB (PDGF-BB) to induce the phenotypic switch of VSMCs. Histological AVF changes are analyzed using hematoxylin-eosin. Western blot and quantitative real-time polymerase chain reaction (qRT-PCR) are utilized to detect prostaglandin-endoperoxide synthase 2 (PTGS2) expression. In vivo, luteolin inhibits neointima formation and reduces vimentin, α-SMA, MCP-1, MMP-9, TNF-α, and IL-6 levels. In vitro, under PDGF-BB treatment, luteolin inhibits proliferation and migration and reduces TNF-α, vimentin, α-SMA, MCP-1, MMP-9, and IL-6 levels in VSMCs. In rat AVF tissues, PTGS2 expression is increased. Luteolin inhibits PTGS2 expression in vivo and in vitro. PTGS2 overexpression reverses the role of luteolin in extracellular matrix protein expression, proliferation, inflammation, and migration in VSMCs treated with PDGF-BB. Altogether, in the AVF, luteolin inhibits proliferation, migration, the phenotypic switch of VSMCs, neointima formation, and the inflammatory response through inhibiting PTGS2 expression.

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来源期刊
Advanced biology
Advanced biology Biochemistry, Genetics and Molecular Biology-Biochemistry, Genetics and Molecular Biology (all)
CiteScore
6.60
自引率
0.00%
发文量
130
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