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减少内源性不稳定锌可能有助于减少血管支架周围平滑肌细胞损伤。

Reducing Endogenous Labile Zn May Help to Reduce Smooth Muscle Cell Injury around Vascular Stents.

机构信息

Key Laboratory of Advanced Technology of Materials, Ministry of Education, School of Materials Science and Engineering, Southwest Jiaotong University, Chengdu 610031, China.

Medical College of Acu-Moxi and Rehabilitation, Guanzhou University of Chinese Medicine, Guangzhou 510006, China.

出版信息

Int J Mol Sci. 2022 May 5;23(9):5139. doi: 10.3390/ijms23095139.

DOI:10.3390/ijms23095139
PMID:35563532
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9101291/
Abstract

Vascular stent service involves complex service environments and performance requirements, among which the histocompatibility of the stent could seriously affect the therapeutic effect. In the pathology of vascular disease, the thin fiber cap is easily ruptured, exposing the necrotic core below, and triggering a series of dangerous biochemical reactions. In contrast, the thin neointima, considered an essential structure growing on the stent, may evolve into vulnerable plaque structures due to lesions induced by the stent. Therefore, the reduction of necrosis around the stent below the thin neointima is indispensable. In this work, different cell model experiments suggested that the content of endogenous labile Zn positively correlated with cell injury. Zinquin-Zn fluorescence experiments and zinc ion channels research suggested that the change in the content of endogenous labile Zn in smooth muscle cells is affected by different stent coatings. The content of endogenous labile Zn in cells negatively correlated with cell viability. Animal experiments indirectly verified the increase in endogenous labile Zn by detecting the expression of Zn regulatory protein (metallothionein) in the necrotic tissues. Reducing the content of endogenous labile Zn may favor a reduction in smooth muscle cell injury and necrosis. This biochemical mechanism is effective in improving the therapeutic effect of vascular stents.

摘要

血管支架服务涉及复杂的服务环境和性能要求,其中支架的组织相容性可能严重影响治疗效果。在血管疾病的病理学中,薄纤维帽容易破裂,暴露出下面的坏死核心,并引发一系列危险的生化反应。相比之下,薄的新生内膜被认为是支架上生长的必不可少的结构,但由于支架引起的损伤,可能会演变成易损斑块结构。因此,减少支架下方薄新生内膜周围的坏死是必不可少的。在这项工作中,不同的细胞模型实验表明,内源性不稳定锌的含量与细胞损伤呈正相关。Zinquin-Zn 荧光实验和锌离子通道研究表明,平滑肌细胞中内源性不稳定锌含量的变化受不同支架涂层的影响。细胞内源性不稳定锌的含量与细胞活力呈负相关。动物实验通过检测坏死组织中锌调节蛋白(金属硫蛋白)的表达间接证实了内源性不稳定锌的增加。减少内源性不稳定锌的含量可能有利于减少平滑肌细胞损伤和坏死。这种生化机制可有效提高血管支架的治疗效果。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c7c/9101291/7d482b58869d/ijms-23-05139-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c7c/9101291/b8bc915ae0ba/ijms-23-05139-g001.jpg
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