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Yiqihuoxuejiedu Formula Restrains Vascular Remodeling by Reducing the Inflammation Reaction and Cx43 Expression in the Adventitia after Balloon Injury

机译:Yiqihuoxuejiedu公式通过减少气球损伤后的外膜中的炎症反应和CX43表达来限制血管重塑

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摘要

Vascular remodeling is closely related to hypertension, atherosclerosis, and restenosis after PCI. Considerable evidence indicates that the activation and proliferation of adventitial fibroblasts play key roles in vessel injury. The inflammatory response and high expression of connexins contribute to adventitial remodeling. Therefore, reducing inflammation reaction and connexins expression in adventitia may become a new target to prevent vascular remodeling. Yiqihuoxuejiedu formula, composed of TCM therapeutic principle of supplementing qi, activating blood and detoxification, can inhibit restenosis after intimal injury. To further investigate the effect of Yiqihuoxuejiedu formula on inflammation and connexins, we established a carotid artery injury model. In model rats, hyperplasia in the intima was mild but obvious in the adventitia; CRP heightened; expressions of MCP-1, CD68, and Cx43 increased. Yiqihuoxuejiedu formula relieved intimal hyperplasia and adventitial area, obviously diminished the expressions of CD68 and Cx43 in the adventitia, and reduced CRP but did not lower MCP-1. These results indicated that Yiqihuoxuejiedu formula inhibited vascular remodeling especially adventitial hyperplasia by reducing the inflammation reaction including lowering macrophages infiltration and systemic nonspecific inflammatory response and also restraining gap junction connexins leading to less communication among cells. This study provides new ideas and methods for the prevention and treatment of vascular remodeling.
机译:血管重塑与PCI后高血压,动脉粥样硬化和再狭窄密切相关。相当大的证据表明,过度成纤维细胞的激活和增殖在血管损伤中发挥关键作用。 Connexins的炎症反应和高表达有助于过度重塑。因此,减少去除症中的炎症反应和Connexins表达可能成为预防血管重塑的新靶标。 Yiqihuoxuejiedu公式,由TCM治疗原理补充QI,激活血液和排毒,可以抑制内膜损伤后的再狭窄。为了进一步探讨益青昔苏岛公式对炎症和连接蛋白的影响,我们建立了一种颈动脉损伤模型。在模型大鼠中,内膜中的增生是温和但在外面的情况下显而易见; CRP加剧; MCP-1,CD68和CX43的表达增加。益桥汇津津司配方缓解了内膜增生和过度面积,明显减少了CD68和CX43的表达,并减少了CRP,但没有降低MCP-1。这些结果表明,益季欧夏津津型通过降低炎症反应,尤其卓昔苏岛公式抑制血管重塑,特别是过度增生,包括降低巨噬细胞浸润和全身非特异性炎症反应,以及限制间隙结XExxins导致细胞之间的沟通较少。本研究为预防和治疗血管改造提供了新的思路和方法。

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