Dietary modifications affect renal recovery during the healing phase following ischemic acute ischemic kidney injury.

IF 4.6 2区 生物学 Q2 CELL BIOLOGY
Frontiers in Cell and Developmental Biology Pub Date : 2025-05-22 eCollection Date: 2025-01-01 DOI:10.3389/fcell.2025.1494660
Junseok Jeon, Kyungho Lee, Hojin Jeon, Kyeong Eun Yang, Cheol-Jung Lee, Jung Eun Lee, Ghee Young Kwon, Wooseong Huh, Hye Ryoun Jang
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Abstract

Introduction: The effects of dietary modifications, such as varying amounts of salt, fat, and protein intake on the healing phase of acute kidney injury (AKI) remain to be elucidated. We investigated the effects of low- or high-salt/fat/protein diets on the intrarenal immunologic micromilieu and healing after renal ischemia-reperfusion injury (IRI) using murine ischemic AKI and human kidney-2 (HK-2) cell hypoxia models.

Methods: Three cohorts of male C57BL/6 mice (9-weeks old) were fed the designated diet from the third day following renal IRI until sacrifice (6 or 12 weeks after bilateral or unilateral IRI, respectively) in groups as follows: cohort 1, control, high- and low-salt/fat/protein; cohort 2, control, high- and low-salt; cohort 3, control, high- and low-fat/protein. Hypoxic HK-2 cells were treated with sodium chloride, amino acids, or fatty acids.

Results: Low-salt/fat/protein diet aggravated interstitial fibrosis, enhanced TGF-β expression, and induced more proinflammatory changes after bilateral IRI. High-salt diet aggravated renal tubular damage and enhanced the expression of intrarenal TGF-β after bilateral IRI, whereas low-salt diet enhanced the expression of intrarenal TGF-β after unilateral IRI. Low-salt diet induced more proinflammatory changes after bilateral IRI. Blood urea nitrogen levels were lower in the low fat/protein group than that in the control group following IRI. However, low-fat/protein diet aggravated interstitial fibrosis and enhanced intrarenal TGF-β expression after unilateral IRI. High sodium- or protein-containing media suppressed the proliferation of hypoxic HK-2 cells, whereas high lipid-containing media enhanced the proliferation of hypoxic HK-2 cells.

Conclusion: Excessive low or high salt, low fat, and low protein diet may adversely affect the healing process following renal IRI, supporting the importance of adequate and balanced nutrition during the recovery phase of ischemic AKI.

饮食改变影响急性缺血性肾损伤愈合期的肾脏恢复。
饮食改变,如不同量的盐、脂肪和蛋白质摄入对急性肾损伤(AKI)愈合期的影响仍有待阐明。我们采用小鼠缺血性AKI和人肾-2 (HK-2)细胞缺氧模型,研究了低盐/高脂/高蛋白饮食对肾内免疫微环境和肾缺血再灌注损伤(IRI)后愈合的影响。方法:3组雄性C57BL/6小鼠(9周龄)从肾脏IRI发生后第3天起(分别为双侧或单侧IRI发生后6周或12周)饲喂指定的饮食,分为以下组:队列1,对照组,高盐/脂肪/蛋白质组和低盐/脂肪/蛋白质组;队列2,对照组,高盐和低盐;队列3,对照组,高脂和低脂/蛋白质。缺氧HK-2细胞分别用氯化钠、氨基酸或脂肪酸处理。结果:低盐/低脂/低蛋白饮食加重了双侧IRI后间质纤维化,TGF-β表达增强,促炎改变增多。高盐饮食加重双侧IRI后肾小管损伤,提高肾内TGF-β表达,而低盐饮食提高单侧IRI后肾内TGF-β表达。低盐饮食诱导双侧IRI后更多的促炎改变。IRI后,低脂/蛋白组的血尿素氮水平低于对照组。然而,低脂/蛋白饮食加重了单侧IRI后间质纤维化,增强了肾内TGF-β的表达。高钠或高蛋白培养基抑制缺氧HK-2细胞的增殖,而高脂培养基促进缺氧HK-2细胞的增殖。结论:过度的低盐或高盐、低脂肪和低蛋白饮食可能对肾IRI后的愈合过程产生不利影响,支持在缺血性AKI恢复期充足和均衡营养的重要性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Frontiers in Cell and Developmental Biology
Frontiers in Cell and Developmental Biology Biochemistry, Genetics and Molecular Biology-Cell Biology
CiteScore
9.70
自引率
3.60%
发文量
2531
审稿时长
12 weeks
期刊介绍: Frontiers in Cell and Developmental Biology is a broad-scope, interdisciplinary open-access journal, focusing on the fundamental processes of life, led by Prof Amanda Fisher and supported by a geographically diverse, high-quality editorial board. The journal welcomes submissions on a wide spectrum of cell and developmental biology, covering intracellular and extracellular dynamics, with sections focusing on signaling, adhesion, migration, cell death and survival and membrane trafficking. Additionally, the journal offers sections dedicated to the cutting edge of fundamental and translational research in molecular medicine and stem cell biology. With a collaborative, rigorous and transparent peer-review, the journal produces the highest scientific quality in both fundamental and applied research, and advanced article level metrics measure the real-time impact and influence of each publication.
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