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高外源性抗氧化剂心脏修复疗法预防心力衰竭六个阶段:心脏饮食法

High Exogenous Antioxidant, Restorative Treatment (Heart) for Prevention of the Six Stages of Heart Failure: The Heart Diet.

作者信息

Singh Ram B, Fedacko Jan, Pella Dominik, Fatima Ghizal, Elkilany Galal, Moshiri Mahmood, Hristova Krasimira, Jakabcin Patrik, Vaňova Natalia

机构信息

Halberg Hospital and Research Institute, Moradabad 244001, India.

Department of Gerontology and Geriatric, Medipark, University Research Park, PJ Safarik University, 040-11 Kosice, Slovakia.

出版信息

Antioxidants (Basel). 2022 Jul 27;11(8):1464. doi: 10.3390/antiox11081464.

DOI:10.3390/antiox11081464
PMID:36009183
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9404840/
Abstract

The exact pathophysiology of heart failure (HF) is not yet known. Western diet, characterized by highly sweetened foods, as well as being rich in fat, fried foods, red meat and processed meat, eggs, and sweet beverages, may cause inflammation, leading to oxidative dysfunction in the cardiac ultra-structure. Oxidative function of the myocardium and how oxidative dysfunction causes physio-pathological remodeling, leading to HF, is not well known. Antioxidants, such as polyphenolics and flavonoids, omega-3 fatty acids, and other micronutrients that are rich in Indo-Mediterranean-type diets, could be protective in sustaining the oxidative functions of the heart. The cardiomyocytes use glucose and fatty acids for the physiological functions depending upon the metabolic requirements of the heart. Apart from toxicity due to glucose, lipotoxicity also adversely affects the cardiomyocytes, which worsen in the presence of deficiency of endogenous antioxidants and deficiency of exogenous antioxidant nutrients in the diet. The high-sugar-and-high-fat-induced production of ceramide, advanced glycation end products (AGE) and triamino-methyl-N-oxide (TMAO) can predispose individuals to oxidative dysfunction and Ca-overloading. The alteration in the biology may start with normal cardiac cell remodeling to biological remodeling due to inflammation. An increase in the fat content of a diet in combination with inducible nitric oxide synthase (NOSi) via N-arginine methyl ester has been found to preserve the ejection fraction in HF. It is proposed that a greater intake of high exogenous antioxidant restorative treatment (HEART) diet, polyphenolics and flavonoids, as well as cessation of red meat intake and egg, can cause improvement in the oxidative function of the heart, by inhibiting oxidative damage to lipids, proteins and DNA in the cell, resulting in beneficial effects in the early stage of the Six Stages of HF. There is an unmet need to conduct cohort studies and randomized, controlled studies to demonstrate the role of the HEART diet in the treatment of HF.

摘要

心力衰竭(HF)的确切病理生理学尚不清楚。西方饮食以高糖食物为特征,同时富含脂肪、油炸食品、红肉、加工肉类、鸡蛋和甜饮料,可能会引发炎症,导致心脏超微结构中的氧化功能障碍。心肌的氧化功能以及氧化功能障碍如何导致生理病理重塑进而引发心力衰竭,目前尚不清楚。抗氧化剂,如多酚类和黄酮类、ω-3脂肪酸以及其他富含印度-地中海型饮食的微量营养素,可能对维持心脏的氧化功能具有保护作用。心肌细胞根据心脏的代谢需求利用葡萄糖和脂肪酸来实现生理功能。除了葡萄糖毒性外,脂毒性也会对心肌细胞产生不利影响,在内源性抗氧化剂缺乏和饮食中外源性抗氧化营养物质缺乏的情况下,这种影响会更加严重。高糖高脂诱导产生的神经酰胺、晚期糖基化终产物(AGE)和三甲胺-N-氧化物(TMAO)会使个体易患氧化功能障碍和钙超载。生物学上的改变可能始于正常的心脏细胞重塑,进而因炎症发展为生物学重塑。研究发现,通过N-精氨酸甲酯增加饮食中的脂肪含量并联合诱导型一氧化氮合酶(NOSi)可维持心力衰竭患者的射血分数。有人提出,增加高外源性抗氧化修复治疗(HEART)饮食、多酚类和黄酮类的摄入量,以及停止摄入红肉和鸡蛋,可通过抑制细胞内脂质、蛋白质和DNA的氧化损伤来改善心脏的氧化功能,从而在心力衰竭六个阶段的早期产生有益效果。目前仍需要进行队列研究和随机对照研究,以证明HEART饮食在心力衰竭治疗中的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10cb/9404840/88f31f2fcaca/antioxidants-11-01464-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10cb/9404840/9c3117be33b6/antioxidants-11-01464-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10cb/9404840/5ba9a34ab800/antioxidants-11-01464-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10cb/9404840/09eaad042a29/antioxidants-11-01464-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10cb/9404840/88f31f2fcaca/antioxidants-11-01464-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10cb/9404840/9c3117be33b6/antioxidants-11-01464-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10cb/9404840/5ba9a34ab800/antioxidants-11-01464-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10cb/9404840/09eaad042a29/antioxidants-11-01464-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10cb/9404840/88f31f2fcaca/antioxidants-11-01464-g004.jpg

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