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饮食调整会影响缺血性急性肾损伤愈合期的肾脏恢复。

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

作者信息

Jeon Junseok, Lee Kyungho, Jeon Hojin, Yang Kyeong Eun, Lee Cheol-Jung, Lee Jung Eun, Kwon Ghee Young, Huh Wooseong, Jang Hye Ryoun

机构信息

Division of Nephrology, Department of Medicine, Samsung Medical Center, Cell and Gene Therapy Institute, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea.

Division of Scientific Instrumentation & Management, Korea Basic Science Institute, Daejeon, Republic of Korea.

出版信息

Front Cell Dev Biol. 2025 May 22;13:1494660. doi: 10.3389/fcell.2025.1494660. eCollection 2025.

DOI:10.3389/fcell.2025.1494660
PMID:40476004
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12137256/
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.

摘要

引言

饮食调整，如不同量的盐、脂肪和蛋白质摄入对急性肾损伤（AKI）愈合阶段的影响仍有待阐明。我们使用小鼠缺血性AKI模型和人肾-2（HK-2）细胞缺氧模型，研究了低盐/高脂/低蛋白或高盐/高脂/高蛋白饮食对肾内免疫微环境及肾缺血再灌注损伤（IRI）后愈合的影响。

方法

三组9周龄雄性C57BL/6小鼠在肾IRI后第三天开始喂食指定饮食，直至处死（分别在双侧或单侧IRI后6周或12周），分组如下：第1组，对照、高盐/高脂/高蛋白和低盐/高脂/低蛋白；第2组，对照、高盐和低盐；第3组，对照、高脂肪/高蛋白和低脂肪/高蛋白。用氯化钠、氨基酸或脂肪酸处理缺氧的HK-2细胞。

结果

低盐/高脂/低蛋白饮食加重双侧IRI后的间质纤维化，增强TGF-β表达，并诱导更多促炎变化。高盐饮食加重双侧IRI后的肾小管损伤并增强肾内TGF-β表达，而低盐饮食增强单侧IRI后肾内TGF-β表达。低盐饮食在双侧IRI后诱导更多促炎变化。IRI后低脂/低蛋白组的血尿素氮水平低于对照组。然而，低脂/低蛋白饮食加重单侧IRI后的间质纤维化并增强肾内TGF-β表达。高钠或高蛋白培养基抑制缺氧HK-2细胞的增殖，而高脂培养基增强缺氧HK-2细胞的增殖。

结论

过多的低盐或高盐、低脂和低蛋白饮食可能对肾IRI后的愈合过程产生不利影响，支持了缺血性AKI恢复阶段充足和均衡营养的重要性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e2b2/12137256/a8e8a267b2ff/fcell-13-1494660-g013.jpg
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