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左旋肉碱治疗可减轻单侧输尿管梗阻引起的肾间质纤维化。

L-carnitine treatment attenuates renal tubulointerstitial fibrosis induced by unilateral ureteral obstruction.

机构信息

Department of Nephrology, Yanbian University Hospital, Yanji, China.

Health Examination Center, Yanbian University Hospital, Yanji, China.

出版信息

Korean J Intern Med. 2021 Mar;36(Suppl 1):S180-S195. doi: 10.3904/kjim.2019.413. Epub 2020 Sep 18.

DOI:10.3904/kjim.2019.413
PMID:32942841
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8009152/
Abstract

BACKGROUND/AIMS: Accumulating evidence indicates that L-carnitine (LC) protects against multiorgan damage through its antioxidant properties and preservation of the mitochondria. Little information is available about the effects of LC on renal fibrosis. This study examined whether LC treatment would provide renoprotection in a rat model of unilateral ureteral obstruction (UUO) and in vitro.

METHODS

Sprague-Dawley rats that underwent UUO were treated daily with LC for 7 or 14 days. The influence of LC on renal injury caused by UUO was evaluated by histopathology, and analysis of gene expression, oxidative stress, mitochondrial function, programmed cell death, and phosphatidylinositol 3-kinase (PI3K)/ AKT/forkhead box protein O 1a (FoxO1a) signaling. In addition, H2O2-exposed human kidney cells (HK-2) were treated with LC.

RESULTS

LC treatment inhibited expression of proinflammatory and profibrotic cytokines, and was followed by a significant attenuation of tubulointerstitial inflammation and fibrosis. The increased oxidative stress caused by UUO was associated with mitochondrial dysfunction and excessive apoptosis and autophagy via PI3K/AKT/FoxO1a-dependent signaling, and this was abrogated by administration of LC. In H2O2-exposed HK-2 cells, LC decreased intracellular production of reactive oxygen species, and suppressed expression of profibrotic cytokines and reduced the number of apoptotic cells.

CONCLUSION

LC protects against the progression of tubulointerstitial fibrosis in an obstructed kidney.

摘要

背景/目的：越来越多的证据表明，左旋肉碱（LC）通过其抗氧化特性和对线粒体的保护作用来防止多器官损伤。关于 LC 对肾纤维化的影响的信息很少。本研究在单侧输尿管梗阻（UUO）大鼠模型中和体外研究了 LC 治疗是否会提供肾脏保护作用。

方法

接受 UUO 的 Sprague-Dawley 大鼠每天接受 LC 治疗 7 或 14 天。通过组织病理学、基因表达分析、氧化应激、线粒体功能、程序性细胞死亡和磷脂酰肌醇 3-激酶（PI3K）/ AKT/叉头框蛋白 O1a（FoxO1a）信号通路分析来评估 LC 对 UUO 引起的肾损伤的影响。此外，用 LC 处理过氧化氢暴露的人肾细胞（HK-2）。

结果

LC 治疗抑制了促炎和促纤维化细胞因子的表达，随后肾小管间质炎症和纤维化明显减轻。UUO 引起的氧化应激增加与线粒体功能障碍以及通过 PI3K/AKT/FoxO1a 依赖性信号通路引起的细胞凋亡和自噬过度有关，而 LC 的给药则阻断了这一过程。在过氧化氢暴露的 HK-2 细胞中，LC 减少了细胞内活性氧的产生，抑制了促纤维化细胞因子的表达，并减少了凋亡细胞的数量。

结论

LC 可防止梗阻性肾脏中肾小管间质纤维化的进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea30/8009152/da8c5940033e/kjim-2019-413f12.jpg
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