文献检索文档翻译深度研究
Suppr Zotero 插件Zotero 插件
邀请有礼套餐&价格历史记录

新学期,新优惠

限时优惠:9月1日-9月22日

30天高级会员仅需29元

1天体验卡首发特惠仅需5.99元

了解详情
不再提醒
插件&应用
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
高级版
套餐订阅购买积分包
AI 工具
文献检索文档翻译深度研究
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 @ 2025

聚酰胺-胺型羟基树枝状大分子(PAMAM-OH)与血管紧张素(1-7)的复合物可预防小鼠因废用引起的骨骼肌萎缩。

The complex of PAMAM-OH dendrimer with Angiotensin (1-7) prevented the disuse-induced skeletal muscle atrophy in mice.

作者信息

Márquez-Miranda Valeria, Abrigo Johanna, Rivera Juan Carlos, Araya-Durán Ingrid, Aravena Javier, Simon Felipe, Pacheco Nicolás, González-Nilo Fernando Danilo, Cabello-Verrugio Claudio

机构信息

Center for Bioinformatics and Integrative Biology (CBIB), Facultad de Ciencias Biologicas, Universidad Andres Bello, Santiago; Fundación Fraunhofer Chile Research, Las Condes.

Departamento de Ciencias Biologicas, Facultad de Ciencias Biologicas & Facultad de Medicina, Universidad Andres Bello; Millennium Institute on Immunology and Immunotherapy, Santiago.

出版信息

Int J Nanomedicine. 2017 Mar 13;12:1985-1999. doi: 10.2147/IJN.S125521. eCollection 2017.


DOI:10.2147/IJN.S125521
PMID:28331320
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5357082/
Abstract

Angiotensin (1-7) (Ang-(1-7)) is a bioactive heptapeptide with a short half-life and has beneficial effects in several tissues - among them, skeletal muscle - by preventing muscle atrophy. Dendrimers are promising vehicles for the protection and transport of numerous bioactive molecules. This work explored the use of a neutral, non-cytotoxic hydroxyl-terminated poly(amidoamine) (PAMAM-OH) dendrimer as an Ang-(1-7) carrier. Bioinformatics analysis showed that the Ang-(1-7)-binding capacity of the dendrimer presented a 2:1 molar ratio. Molecular dynamics simulation analysis revealed the capacity of neutral PAMAM-OH to protect Ang-(1-7) and form stable complexes. The peptide coverage ability of the dendrimer was between ~50% and 65%. Furthermore, an electrophoretic mobility shift assay demonstrated that neutral PAMAM-OH effectively bonded peptides. Experimental results showed that the Ang-(1-7)/PAMAM-OH complex, but not Ang-(1-7) alone, had an anti-atrophic effect when administered intraperitoneally, as evaluated by muscle strength, fiber diameter, myofibrillar protein levels, and atrogin-1 and MuRF-1 expressions. The results of the Ang-(1-7)/PAMAM-OH complex being intraperitoneally injected were similar to the results obtained when Ang-(1-7) was systemically administered through mini-osmotic pumps. Together, the results suggest that Ang-(1-7) can be protected for PAMAM-OH when this complex is intraperitoneally injected. Therefore, the Ang-(1-7)/PAMAM-OH complex is an efficient delivery method for Ang-(1-7), since it improves the anti-atrophic activity of this peptide in skeletal muscle.

摘要

血管紧张素(1-7)(Ang-(1-7))是一种半衰期较短的生物活性七肽,通过预防肌肉萎缩,对包括骨骼肌在内的多种组织具有有益作用。树枝状大分子是用于保护和运输众多生物活性分子的有前景的载体。这项工作探索了使用中性、无细胞毒性的羟基封端聚(酰胺胺)(PAMAM-OH)树枝状大分子作为Ang-(1-7)的载体。生物信息学分析表明,树枝状大分子与Ang-(1-7)的结合能力呈现2:1的摩尔比。分子动力学模拟分析揭示了中性PAMAM-OH保护Ang-(1-7)并形成稳定复合物的能力。树枝状大分子的肽覆盖能力在约50%至65%之间。此外,电泳迁移率变动分析表明中性PAMAM-OH能有效结合肽。实验结果表明,通过肌肉力量、纤维直径、肌原纤维蛋白水平以及atrogin-1和MuRF-1表达评估,腹腔注射时,Ang-(1-7)/PAMAM-OH复合物而非单独的Ang-(1-7)具有抗萎缩作用。腹腔注射Ang-(1-7)/PAMAM-OH复合物的结果与通过微型渗透泵全身给药Ang-(1-7)时获得的结果相似。总之,结果表明腹腔注射该复合物时,Ang-(1-7)可被PAMAM-OH保护。因此,Ang-(1-7)/PAMAM-OH复合物是一种有效的Ang-(1-7)递送方法,因为它提高了该肽在骨骼肌中的抗萎缩活性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/642c/5357082/16080901b517/ijn-12-1985Fig8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/642c/5357082/300e418ff85b/ijn-12-1985Fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/642c/5357082/2f51afbedde5/ijn-12-1985Fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/642c/5357082/30dd0626c672/ijn-12-1985Fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/642c/5357082/ff2e6bd506d1/ijn-12-1985Fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/642c/5357082/41d0175c6492/ijn-12-1985Fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/642c/5357082/abfd9afb2151/ijn-12-1985Fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/642c/5357082/07b3e6e53df4/ijn-12-1985Fig7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/642c/5357082/16080901b517/ijn-12-1985Fig8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/642c/5357082/300e418ff85b/ijn-12-1985Fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/642c/5357082/2f51afbedde5/ijn-12-1985Fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/642c/5357082/30dd0626c672/ijn-12-1985Fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/642c/5357082/ff2e6bd506d1/ijn-12-1985Fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/642c/5357082/41d0175c6492/ijn-12-1985Fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/642c/5357082/abfd9afb2151/ijn-12-1985Fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/642c/5357082/07b3e6e53df4/ijn-12-1985Fig7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/642c/5357082/16080901b517/ijn-12-1985Fig8.jpg

相似文献

[1]
The complex of PAMAM-OH dendrimer with Angiotensin (1-7) prevented the disuse-induced skeletal muscle atrophy in mice.

Int J Nanomedicine. 2017-3-13

[2]
Angiotensin-(1-7) attenuates disuse skeletal muscle atrophy in mice via its receptor, Mas.

Dis Model Mech. 2016-4

[3]
Angiotensin-(1-7) decreases skeletal muscle atrophy induced by angiotensin II through a Mas receptor-dependent mechanism.

Clin Sci (Lond). 2015-3

[4]
Angiotensin-(1-7) Prevents Skeletal Muscle Atrophy Induced by Transforming Growth Factor Type Beta (TGF-β) via Mas Receptor Activation.

Cell Physiol Biochem. 2016

[5]
Protective Effect of Angiotensin 1-7 on Sarcopenia Induced by Chronic Liver Disease in Mice.

Int J Mol Sci. 2020-5-29

[6]
Angiotensin (1-7) Decreases Myostatin-Induced NF-κB Signaling and Skeletal Muscle Atrophy.

Int J Mol Sci. 2020-2-10

[7]
Endotoxin-induced skeletal muscle wasting is prevented by angiotensin-(1-7) through a p38 MAPK-dependent mechanism.

Clin Sci (Lond). 2015-5-19

[8]
Branched-chain amino acids reduce hindlimb suspension-induced muscle atrophy and protein levels of atrogin-1 and MuRF1 in rats.

Nutr Res. 2012-9-17

[9]
Unveiling the G4-PAMAM capacity to bind and protect Ang-(1-7) bioactive peptide by molecular dynamics simulations.

J Comput Aided Mol Des. 2022-9

[10]
IGF-1 prevents ANG II-induced skeletal muscle atrophy via Akt- and Foxo-dependent inhibition of the ubiquitin ligase atrogin-1 expression.

Am J Physiol Heart Circ Physiol. 2010-3-12

引用本文的文献

[1]
Targeted Bioluminescent Imaging of Pancreatic Ductal Adenocarcinoma Using Nanocarrier-Complexed EGFR-Binding Affibody-Gaussia Luciferase Fusion Protein.

Pharmaceutics. 2023-7-19

[2]
Mitigating Cardiotoxicity of Dendrimers: Angiotensin-(1-7) via Its Mas Receptor Ameliorates PAMAM-Induced Cardiac Dysfunction in the Isolated Mammalian Heart.

Pharmaceutics. 2022-12-1

[3]
Nanomedicine for Treating Muscle Dystrophies: Opportunities, Challenges, and Future Perspectives.

Int J Mol Sci. 2022-10-10

[4]
COVID-19 as a Potential Cause of Muscle Injuries in Professional Italian Serie A Soccer Players: A Retrospective Observational Study.

Int J Environ Res Public Health. 2022-9-5

[5]
Unraveling Muscle Impairment Associated With COVID-19 and the Role of 3D Culture in Its Investigation.

Front Nutr. 2022-2-10

[6]
Nanomedicine for Gene Delivery and Drug Repurposing in the Treatment of Muscular Dystrophies.

Pharmaceutics. 2021-2-19

[7]
ACE2, angiotensin 1-7 and skeletal muscle: review in the era of COVID-19.

Clin Sci (Lond). 2020-11-27

[8]
Sarcopenia Induced by Chronic Liver Disease in Mice Requires the Expression of the Bile Acids Membrane Receptor TGR5.

Int J Mol Sci. 2020-10-25

[9]
Protective Effect of Angiotensin 1-7 on Sarcopenia Induced by Chronic Liver Disease in Mice.

Int J Mol Sci. 2020-5-29

[10]
Angiotensin (1-7) Decreases Myostatin-Induced NF-κB Signaling and Skeletal Muscle Atrophy.

Int J Mol Sci. 2020-2-10

本文引用的文献

[1]
Angiotensin-(1-7) attenuates disuse skeletal muscle atrophy in mice via its receptor, Mas.

Dis Model Mech. 2016-4

[2]
Effect of Terminal Groups of Dendrimers in the Complexation with Antisense Oligonucleotides and Cell Uptake.

Nanoscale Res Lett. 2016-12

[3]
Transforming growth factor type beta (TGF-β) requires reactive oxygen species to induce skeletal muscle atrophy.

Cell Signal. 2016-5

[4]
Biomimetics: From Bioinformatics to Rational Design of Dendrimers as Gene Carriers.

PLoS One. 2015-9-18

[5]
ACE2 and vasoactive peptides: novel players in cardiovascular/renal remodeling and hypertension.

Ther Adv Cardiovasc Dis. 2015-8

[6]
Endotoxin-induced skeletal muscle wasting is prevented by angiotensin-(1-7) through a p38 MAPK-dependent mechanism.

Clin Sci (Lond). 2015-5-19

[7]
Role of non-classical renin-angiotensin system axis in renal fibrosis.

Front Physiol. 2015-4-21

[8]
Angiotensins as therapeutic targets beyond heart disease.

Trends Pharmacol Sci. 2015-4-3

[9]
Renin-angiotensin system: an old player with novel functions in skeletal muscle.

Med Res Rev. 2015-3-11

[10]
The angiotensin-(1-7)/Mas axis reduces myonuclear apoptosis during recovery from angiotensin II-induced skeletal muscle atrophy in mice.

Pflugers Arch. 2015-9

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

推荐工具

医学文档翻译智能文献检索