• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

沉默利钠肽-β可减轻自发性高血压大鼠的心血管重塑和高血压。

Silencing salusin-β attenuates cardiovascular remodeling and hypertension in spontaneously hypertensive rats.

机构信息

Key Laboratory of Cardiovascular Disease and Molecular Intervention, Department of Physiology, Nanjing Medical University, Nanjing, Jiangsu 211166, China.

Department of Pathophysiology, Nanjing Medical University, Nanjing, Jiangsu 211166, China.

出版信息

Sci Rep. 2017 Feb 23;7:43259. doi: 10.1038/srep43259.

DOI:10.1038/srep43259
PMID:28230187
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5322393/
Abstract

Salusin-β is a bioactive peptide involved in vascular smooth muscle cell proliferation, vascular fibrosis and hypertension. The present study was designed to determine the effects of silencing salusin-β on hypertension and cardiovascular remodeling in spontaneously hypertensive rats (SHR). Thirteen-week-old male SHR and normotensive Wistar-Kyoto rats (WKY) were subjected to intravenous injection of PBS, adenoviral vectors encoding salusin-β shRNA (Ad-Sal-shRNA) or a scramble shRNA. Salusin-β levels in plasma, myocardium and mesenteric artery were increased in SHR. Silencing salusin-β had no significant effect on blood pressure in WKY, but reduced blood pressure in SHR. It reduced the ratio of left ventricle weight to body weight, cross-sectional areas of cardiocytes and perivascular fibrosis, and decreased the media thickness and the media/lumen ratio of arteries in SHR. Silencing salusin-β almost normalized plasma norepinephrine and angiotensin II levels in SHR. It prevented the upregulation of angiotensin II and AT receptors, and reduced the NAD(P)H oxidase activity and superoxide anion levels in myocardium and mesenteric artery of SHR. Knockdown of salusin-β attenuated cell proliferation and fibrosis in vascular smooth muscle cells from SHR. These results indicate that silencing salusin-β attenuates hypertension and cardiovascular remodeling in SHR.

摘要

沙利素-β是一种参与血管平滑肌细胞增殖、血管纤维化和高血压的生物活性肽。本研究旨在确定沉默沙利素-β对自发性高血压大鼠(SHR)高血压和心血管重构的影响。将 13 周龄雄性 SHR 和正常血压的 Wistar-Kyoto 大鼠(WKY)分别给予 PBS、携带沙利素-β shRNA(Ad-Sal-shRNA)或乱序 shRNA 的腺病毒载体静脉注射。SHR 血浆、心肌和肠系膜动脉中的沙利素-β水平升高。沉默沙利素-β对 WKY 的血压没有显著影响,但降低了 SHR 的血压。它降低了 SHR 左心室重量与体重的比值、心肌细胞的横截面积和血管周围纤维化程度,并降低了 SHR 动脉的中膜厚度和中膜/腔比。沉默沙利素-β几乎使 SHR 血浆去甲肾上腺素和血管紧张素 II 水平正常化。它阻止了心肌和肠系膜动脉中血管紧张素 II 和 AT 受体的上调,并降低了 NAD(P)H 氧化酶活性和超氧阴离子水平。沉默沙利素-β可减轻 SHR 血管平滑肌细胞的增殖和纤维化。这些结果表明,沉默沙利素-β可减轻 SHR 的高血压和心血管重构。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aac/5322393/099a9cec732c/srep43259-f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aac/5322393/69786888aaba/srep43259-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aac/5322393/1dadbe44f140/srep43259-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aac/5322393/081505545a15/srep43259-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aac/5322393/fc0a9efac3a6/srep43259-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aac/5322393/7e4eeb933463/srep43259-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aac/5322393/e7fbead372e0/srep43259-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aac/5322393/e771b3436712/srep43259-f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aac/5322393/099a9cec732c/srep43259-f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aac/5322393/69786888aaba/srep43259-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aac/5322393/1dadbe44f140/srep43259-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aac/5322393/081505545a15/srep43259-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aac/5322393/fc0a9efac3a6/srep43259-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aac/5322393/7e4eeb933463/srep43259-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aac/5322393/e7fbead372e0/srep43259-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aac/5322393/e771b3436712/srep43259-f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aac/5322393/099a9cec732c/srep43259-f8.jpg

相似文献

1
Silencing salusin-β attenuates cardiovascular remodeling and hypertension in spontaneously hypertensive rats.沉默利钠肽-β可减轻自发性高血压大鼠的心血管重塑和高血压。
Sci Rep. 2017 Feb 23;7:43259. doi: 10.1038/srep43259.
2
Silencing salusin β ameliorates heart failure in aged spontaneously hypertensive rats by ROS-relative MAPK/NF-κB pathways in the paraventricular nucleus.沉默利钠肽β通过室旁核内 ROS 相关 MAPK/NF-κB 通路改善老年自发性高血压大鼠心力衰竭。
Int J Cardiol. 2019 Apr 1;280:142-151. doi: 10.1016/j.ijcard.2018.12.020. Epub 2018 Dec 7.
3
A TOR2A Gene Product: Salusin-β Contributes to Attenuated Vasodilatation of Spontaneously Hypertensive Rats.TOR2A 基因产物:salusin-β 导致自发性高血压大鼠血管舒张减弱。
Cardiovasc Drugs Ther. 2021 Feb;35(1):125-139. doi: 10.1007/s10557-020-06983-1.
4
Improvement of Vascular Function by Knockdown of Salusin-β in Hypertensive Rats via Nitric Oxide and Reactive Oxygen Species Signaling Pathway.通过一氧化氮和活性氧信号通路敲低高血压大鼠体内的Salusin-β改善血管功能
Front Physiol. 2021 Apr 9;12:622954. doi: 10.3389/fphys.2021.622954. eCollection 2021.
5
Central blockade of salusin β attenuates hypertension and hypothalamic inflammation in spontaneously hypertensive rats.在自发性高血压大鼠中,salusin β的中枢性阻断可减轻高血压和下丘脑炎症。
Sci Rep. 2015 Jul 29;5:11162. doi: 10.1038/srep11162.
6
Knockdown of Salusin- Improves Cardiovascular Function in Myocardial Infarction-Induced Chronic Heart Failure Rats.沉默素-β 改善心肌梗死后慢性心力衰竭大鼠的心血管功能。
Oxid Med Cell Longev. 2021 Aug 10;2021:8896226. doi: 10.1155/2021/8896226. eCollection 2021.
7
Artificial microRNA interference targeting AT(1a) receptors in paraventricular nucleus attenuates hypertension in rats.靶向室旁核 AT(1a)受体的人工 microRNA 干扰可减轻大鼠高血压。
Gene Ther. 2012 Aug;19(8):810-7. doi: 10.1038/gt.2011.145. Epub 2011 Sep 29.
8
[Effects of RNA interference targeting angiotensin 1 receptor and angiotensin-converting enzyme on blood pressure and myocardial remodeling in spontaneous hypertensive rats].[RNA干扰靶向血管紧张素1受体和血管紧张素转换酶对自发性高血压大鼠血压及心肌重塑的影响]
Zhonghua Xin Xue Guan Bing Za Zhi. 2010 Jan;38(1):60-6.
9
Adverse remodeling of the obtuse marginal artery in compensatory hypertrophied myocardium from spontaneously hypertensive rats.自发性高血压大鼠代偿性肥厚心肌中钝缘支动脉的不良重塑。
Cardiovasc Pathol. 2017 Jan-Feb;26:51-54. doi: 10.1016/j.carpath.2016.11.002. Epub 2016 Nov 12.
10
Salusin β Within the Nucleus Tractus Solitarii Suppresses Blood Pressure Via Inhibiting the Activities of Presympathetic Neurons in the Rostral Ventrolateral Medulla in Spontaneously Hypertensive Rats.孤束核内的Salusin β通过抑制自发性高血压大鼠延髓头端腹外侧区的交感神经节前神经元活动来降低血压。
Cardiovasc Toxicol. 2016 Jul;16(3):223-34. doi: 10.1007/s12012-015-9330-2.

引用本文的文献

1
Downregulation of salusins alleviates hypertrophic cardiomyopathy via attenuating oxidative stress and autophagy.Salusin 的下调通过减轻氧化应激和自噬来缓解肥厚型心肌病。
Eur J Med Res. 2024 Feb 9;29(1):109. doi: 10.1186/s40001-024-01676-z.
2
The Clinical Significance of Salusins in Systemic Sclerosis-A Cross-Sectional Study.Salusins在系统性硬化症中的临床意义——一项横断面研究
Diagnostics (Basel). 2023 Feb 23;13(5):848. doi: 10.3390/diagnostics13050848.
3
Salusin-β, a TOR2A gene product, promotes proliferation, migration, fibrosis, and calcification of smooth muscle cells and accelerates the imbalance of vasomotor function and vascular remodeling in monocrotaline-induced pulmonary hypertensive rats.

本文引用的文献

1
Role of the Renin-Angiotensin-Aldosterone System beyond Blood Pressure Regulation: Molecular and Cellular Mechanisms Involved in End-Organ Damage during Arterial Hypertension.肾素-血管紧张素-醛固酮系统在血压调节之外的作用:动脉高血压期间终末器官损伤所涉及的分子和细胞机制
Int J Mol Sci. 2016 Jun 23;17(7):797. doi: 10.3390/ijms17070797.
2
Resveratrol Inhibition of Rac1-Derived Reactive Oxygen Species by AMPK Decreases Blood Pressure in a Fructose-Induced Rat Model of Hypertension.白藜芦醇通过AMPK抑制Rac1衍生的活性氧,降低果糖诱导的高血压大鼠模型的血压。
Sci Rep. 2016 May 3;6:25342. doi: 10.1038/srep25342.
3
Evidence for a critical role of the sympathetic nervous system in hypertension.
Salusin-β是TOR2A基因的产物,可促进平滑肌细胞的增殖、迁移、纤维化和钙化,并加速野百合碱诱导的肺动脉高压大鼠的血管舒缩功能失衡和血管重塑。
Front Pharmacol. 2022 Sep 30;13:928834. doi: 10.3389/fphar.2022.928834. eCollection 2022.
4
Salusin-β in Intermediate Dorsal Motor Nucleus of the Vagus Regulates Sympathetic-Parasympathetic Balance and Blood Pressure.迷走神经中间背侧运动核中的Salusin-β调节交感-副交感神经平衡和血压。
Biomedicines. 2021 Aug 31;9(9):1118. doi: 10.3390/biomedicines9091118.
5
Knockdown of Salusin- Improves Cardiovascular Function in Myocardial Infarction-Induced Chronic Heart Failure Rats.沉默素-β 改善心肌梗死后慢性心力衰竭大鼠的心血管功能。
Oxid Med Cell Longev. 2021 Aug 10;2021:8896226. doi: 10.1155/2021/8896226. eCollection 2021.
6
3D-printed cranial models simulating operative field depth for microvascular training in neurosurgery.用于神经外科微血管训练的模拟手术视野深度的3D打印颅骨模型。
Surg Neurol Int. 2021 May 10;12:213. doi: 10.25259/SNI_849_2020. eCollection 2021.
7
Improvement of Vascular Function by Knockdown of Salusin-β in Hypertensive Rats via Nitric Oxide and Reactive Oxygen Species Signaling Pathway.通过一氧化氮和活性氧信号通路敲低高血压大鼠体内的Salusin-β改善血管功能
Front Physiol. 2021 Apr 9;12:622954. doi: 10.3389/fphys.2021.622954. eCollection 2021.
8
TLR4 regulates vascular smooth muscle cell proliferation in hypertension via modulation of the NLRP3 inflammasome.Toll样受体4(TLR4)通过调节NLRP3炎性小体来调控高血压中血管平滑肌细胞的增殖。
Am J Transl Res. 2021 Jan 15;13(1):314-325. eCollection 2021.
9
Antihypertensive effects of exercise involve reshaping of gut microbiota and improvement of gut-brain axis in spontaneously hypertensive rat.运动对高血压的影响涉及重塑肠道微生物群,并改善自发性高血压大鼠的肠道-大脑轴。
Gut Microbes. 2021 Jan-Dec;13(1):1-24. doi: 10.1080/19490976.2020.1854642.
10
A TOR2A Gene Product: Salusin-β Contributes to Attenuated Vasodilatation of Spontaneously Hypertensive Rats.TOR2A 基因产物:salusin-β 导致自发性高血压大鼠血管舒张减弱。
Cardiovasc Drugs Ther. 2021 Feb;35(1):125-139. doi: 10.1007/s10557-020-06983-1.
交感神经系统在高血压中起关键作用的证据。
J Am Soc Hypertens. 2016 May;10(5):457-66. doi: 10.1016/j.jash.2016.02.015. Epub 2016 Mar 4.
4
Salusin-β induces foam cell formation and monocyte adhesion in human vascular smooth muscle cells via miR155/NOX2/NFκB pathway.Salusin-β通过miR155/NOX2/NFκB途径诱导人血管平滑肌细胞中泡沫细胞的形成和单核细胞黏附。
Sci Rep. 2016 Mar 23;6:23596. doi: 10.1038/srep23596.
5
Salusin-β Promotes Vascular Smooth Muscle Cell Migration and Intimal Hyperplasia After Vascular Injury via ROS/NFκB/MMP-9 Pathway.沙利素-β通过 ROS/NFκB/MMP-9 通路促进血管损伤后血管平滑肌细胞迁移和内膜增生。
Antioxid Redox Signal. 2016 Jun 20;24(18):1045-57. doi: 10.1089/ars.2015.6475. Epub 2016 Apr 8.
6
Prenatal inflammation-induced NF-κB dyshomeostasis contributes to renin-angiotensin system over-activity resulting in prenatally programmed hypertension in offspring.产前炎症诱导的核因子κB(NF-κB)稳态失调导致肾素-血管紧张素系统过度活跃,从而导致子代出现产前编程性高血压。
Sci Rep. 2016 Feb 15;6:21692. doi: 10.1038/srep21692.
7
New Insights Into Mechanisms Associated With Angiotensin II-Induced Vascular Hypertrophy and Remodeling.血管紧张素II诱导的血管肥大和重塑相关机制的新见解
Hypertension. 2016 Mar;67(3):501-3. doi: 10.1161/HYPERTENSIONAHA.115.06737. Epub 2016 Feb 1.
8
Interleukin-10 deficiency aggravates angiotensin II-induced cardiac remodeling in mice.白细胞介素-10缺乏加重小鼠血管紧张素II诱导的心脏重塑。
Life Sci. 2016 Feb 1;146:214-21. doi: 10.1016/j.lfs.2016.01.022. Epub 2016 Jan 14.
9
Central blockade of salusin β attenuates hypertension and hypothalamic inflammation in spontaneously hypertensive rats.在自发性高血压大鼠中,salusin β的中枢性阻断可减轻高血压和下丘脑炎症。
Sci Rep. 2015 Jul 29;5:11162. doi: 10.1038/srep11162.
10
Oxidative stress and antioxidants in hypertension-a current review.高血压中的氧化应激与抗氧化剂——当前综述
Curr Hypertens Rev. 2015;11(2):132-42. doi: 10.2174/1573402111666150529130922.