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长期给予牛骨胶原蛋白肽对自发性高血压大鼠心肌肥厚的影响。

Effects of Long-Term Administration of Bovine Bone Gelatin Peptides on Myocardial Hypertrophy in Spontaneously Hypertensive Rats.

机构信息

School of Food Science and Engineering, Ningxia University, Yinchuan 750021, China.

Key Lab of Meat Processing and Quality Control, MOE, College of Food Science and Technology, Nanjing Agricultural University, Nanjing 210095, China.

出版信息

Nutrients. 2023 Dec 6;15(24):5021. doi: 10.3390/nu15245021.

DOI:10.3390/nu15245021
PMID:38140281
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10745459/
Abstract

The research purpose was to investigate the effects and the underlying molecular mechanisms of bovine bone gelatin peptides (BGP) on myocardial hypertrophy in spontaneously hypertensive rats (SHR). BGP relieved myocardial hypertrophy and fibrosis in SHR rats in a dose-dependent manner by reducing the left ventricular mass index, myocardial cell diameter, myocardial fibrosis area, and levels of myocardial hypertrophy markers (atrial natriuretic and brain natriuretic peptide). Label-free quantitative proteomics analysis showed that long-term administration of BGP changed the left ventricle proteomes of SHR. The 37 differentially expressed proteins in the high-dose BGP group participated in multiple signaling pathways associated with cardiac hypertrophy and fibrosis indicating that BGP could play a cardioprotective effect on SHR rats by targeting multiple signaling pathways. Further validation experiments showed that a high dose of BGP inhibited the expression of phosphoinositide 3-kinase (Pi3k), phosphorylated protein kinase B (p-Akt), and transforming growth factor-beta 1 (TGF-β1) in the myocardial tissue of SHR rats. Together, BGP could be an effective candidate for functional nutritional supplements to inhibit myocardial hypertrophy and fibrosis by negatively regulating the TGF-β1 and Pi3k/Akt signaling pathways.

摘要

本研究旨在探讨牛骨胶原蛋白肽（BGP）对自发性高血压大鼠（SHR）心肌肥大的作用及其潜在的分子机制。BGP 通过降低左心室质量指数、心肌细胞直径、心肌纤维化面积和心肌肥大标志物（心房利钠肽和脑利钠肽）水平，以剂量依赖的方式缓解 SHR 大鼠的心肌肥大和纤维化。无标记定量蛋白质组学分析表明，BGP 的长期给药改变了 SHR 的左心室蛋白质组。高剂量 BGP 组中 37 个差异表达蛋白参与了多个与心肌肥大和纤维化相关的信号通路，表明 BGP 可能通过靶向多个信号通路对 SHR 大鼠发挥心脏保护作用。进一步的验证实验表明，高剂量 BGP 抑制了 SHR 大鼠心肌组织中磷酸肌醇 3-激酶（Pi3k）、磷酸化蛋白激酶 B（p-Akt）和转化生长因子-β1（TGF-β1）的表达。综上所述，BGP 可作为一种有效的功能性营养补充剂，通过负调控 TGF-β1 和 Pi3k/Akt 信号通路，抑制心肌肥大和纤维化。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53ff/10745459/9423e6964c1c/nutrients-15-05021-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53ff/10745459/00234ee8cba0/nutrients-15-05021-g001a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53ff/10745459/158e1650a2b2/nutrients-15-05021-g002a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53ff/10745459/10841b8406dd/nutrients-15-05021-g003a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53ff/10745459/d7a79d3a0bf6/nutrients-15-05021-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53ff/10745459/e1edb58e5c6f/nutrients-15-05021-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53ff/10745459/9423e6964c1c/nutrients-15-05021-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53ff/10745459/00234ee8cba0/nutrients-15-05021-g001a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53ff/10745459/158e1650a2b2/nutrients-15-05021-g002a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53ff/10745459/10841b8406dd/nutrients-15-05021-g003a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53ff/10745459/d7a79d3a0bf6/nutrients-15-05021-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53ff/10745459/e1edb58e5c6f/nutrients-15-05021-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53ff/10745459/9423e6964c1c/nutrients-15-05021-g006.jpg

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本文引用的文献

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J Agric Food Chem. 2022 Aug 17;70(32):9877-9887. doi: 10.1021/acs.jafc.2c02982. Epub 2022 Aug 2.
2
The physiological activity of bioactive peptides obtained from meat and meat by-products.从肉类和肉类副产物中获得的生物活性肽的生理活性。
Adv Food Nutr Res. 2021;97:147-185. doi: 10.1016/bs.afnr.2021.02.016. Epub 2021 Apr 21.
3
Antihypertensive Effects in Vitro and in Vivo of Novel Angiotensin-Converting Enzyme Inhibitory Peptides from Bovine Bone Gelatin Hydrolysate.
牛骨明胶水解物中新型血管紧张素转化酶抑制肽的体外和体内降压作用。
J Agric Food Chem. 2020 Jan 22;68(3):759-768. doi: 10.1021/acs.jafc.9b05618. Epub 2019 Dec 31.
4
Left ventricular hypertrophy and hypertension.左心室肥厚与高血压。
Prog Cardiovasc Dis. 2020 Jan-Feb;63(1):10-21. doi: 10.1016/j.pcad.2019.11.009. Epub 2019 Nov 21.
5
Proteomics of the Rat Myocardium during Development of Type 2 Diabetes Mellitus Reveals Progressive Alterations in Major Metabolic Pathways.2 型糖尿病大鼠心肌蛋白质组学研究揭示了主要代谢途径的渐进性改变。
J Proteome Res. 2018 Jul 6;17(7):2521-2532. doi: 10.1021/acs.jproteome.8b00276. Epub 2018 Jun 15.
6
Mechanisms of physiological and pathological cardiac hypertrophy.生理性和病理性心肌肥厚的机制。
Nat Rev Cardiol. 2018 Jul;15(7):387-407. doi: 10.1038/s41569-018-0007-y.
7
Exploration of collagen recovered from animal by-products as a precursor of bioactive peptides: Successes and challenges.从动物副产品中回收胶原蛋白作为生物活性肽前体的探索：成功与挑战。
Crit Rev Food Sci Nutr. 2019;59(13):2011-2027. doi: 10.1080/10408398.2018.1436038. Epub 2018 Mar 1.
8
AMPK activation counteracts cardiac hypertrophy by reducing O-GlcNAcylation.AMPK激活通过减少O-连接的N-乙酰葡糖胺化来对抗心脏肥大。
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9
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10
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