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

Authors :
Hai Yan Zhao
Hui Ying Li
Jian Jin
Ji Zhe Jin
Long Ye Zhang
Mei Ying Xuan
Xue Mei Jin
Yu Ji Jiang
Hai Lan Zheng
Ying Shun Jin
Yong Jie Jin
Bum Soon Choi
Chul Woo Yang
Shang Guo Piao
Can Li
Source :
The Korean Journal of Internal Medicine, Vol 36, Iss Suppl 1, Pp S180-S195 (2021)
Publication Year :
2021
Publisher :
The Korean Association of Internal Medicine, 2021.

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

Details

Language :
English
ISSN :
12263303 and 20056648
Volume :
36
Issue :
Suppl 1
Database :
Directory of Open Access Journals
Journal :
The Korean Journal of Internal Medicine
Publication Type :
Academic Journal
Accession number :
edsdoj.f38cca8654bf413aa826b4a8008cf86b
Document Type :
article
Full Text :
https://doi.org/10.3904/kjim.2019.413