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尾加压素Ⅱ通过调控大鼠体内C反应蛋白、单核细胞趋化蛋白-1及转化生长因子-β的表达来改善动脉粥样硬化。

Urantide improves atherosclerosis by controlling C-reactive protein, monocyte chemotactic protein-1 and transforming growth factor-β expression in rats.

作者信息

Zhao Juan, Xie Li-DE, Song Cheng-Jun, Mao Xiao-Xia, Yu Hai-Rong, Yu Quan-Xin, Ren Li-Qun, Shi Yan, Xie Ya-Qin, Li Ying, Liu Sha-Sha, Yang Xiao-Hong

机构信息

School of Pharmaceutical Sciences, Jilin University, Changchun, Jilin 130021, P.R. China ; Department of Pathophysiology, Chengde Medical University, Chengde, Hebei 067000, P.R. China.

Department of Pathophysiology, Chengde Medical University, Chengde, Hebei 067000, P.R. China.

出版信息

Exp Ther Med. 2014 Jun;7(6):1647-1652. doi: 10.3892/etm.2014.1654. Epub 2014 Mar 31.

DOI:10.3892/etm.2014.1654
PMID:24926360
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4043621/
Abstract

The aim of the present study was to investigate the effects of urantide on the expression status of C-reactive protein (CRP) and the inflammatory cytokines monocyte chemotactic protein (MCP)-1 and transforming growth factor (TGF)-β in the aortas of rats with atherosclerosis (AS), and to identify its underlying mechanisms. The effects of urantide in a rat model of AS and in cultured rat vascular smooth muscle cells (VSMCs) were analyzed via hematoxylin and eosin staining, immunohistochemical staining and ELISA. The results demonstrated that urantide downregulated the expression of inflammatory mediators CRP and MCP-1 and upregulated the expression of TGF-β. The results indicated that urantide inhibited the proliferation of VSMCs. In addition, urantide reduced the expression of CRP and downregulated the secretion of TGF-β in the culture supernatant. In conclusion, urantide ameliorated the arterial inflammatory damage that was observed in the AS rat model at the cell and tissue levels by controlling the expression of CRP and the inflammatory cytokines MCP-1 and TGF-β. Therefore, urantide may be a potential agent for the complementary treatment of AS.

摘要

本研究的目的是探讨尿调节素对动脉粥样硬化(AS)大鼠主动脉中C反应蛋白(CRP)、炎性细胞因子单核细胞趋化蛋白(MCP)-1和转化生长因子(TGF)-β表达状态的影响,并确定其潜在机制。通过苏木精-伊红染色、免疫组织化学染色和酶联免疫吸附测定(ELISA)分析尿调节素在AS大鼠模型和培养的大鼠血管平滑肌细胞(VSMC)中的作用。结果表明,尿调节素下调炎性介质CRP和MCP-1的表达,并上调TGF-β的表达。结果表明,尿调节素抑制VSMC的增殖。此外,尿调节素降低了CRP的表达,并下调了培养上清液中TGF-β的分泌。总之,尿调节素通过控制CRP以及炎性细胞因子MCP-1和TGF-β的表达,在细胞和组织水平改善了AS大鼠模型中观察到的动脉炎性损伤。因此,尿调节素可能是AS辅助治疗的一种潜在药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd56/4043621/abbba93e5ee7/ETM-07-06-1647-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd56/4043621/5097c457f9c5/ETM-07-06-1647-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd56/4043621/e61712fba47b/ETM-07-06-1647-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd56/4043621/abbba93e5ee7/ETM-07-06-1647-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd56/4043621/5097c457f9c5/ETM-07-06-1647-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd56/4043621/e61712fba47b/ETM-07-06-1647-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd56/4043621/abbba93e5ee7/ETM-07-06-1647-g02.jpg

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Mol Med Rep. 2021 Apr;23(4). doi: 10.3892/mmr.2021.11923. Epub 2021 Feb 19.
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The peptide compound urantide regulates collagen metabolism in atherosclerotic rat hearts and inhibits the JAK2/STAT3 pathway.肽化合物尿抑胃肽调节动脉粥样硬化大鼠心脏的胶原代谢,并抑制 JAK2/STAT3 通路。
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