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KMID : 0338420210360000180
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The Korean Journal of Internal Medicine
2021 Volume.36 No. 0 p.180 ~ p.195
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L-carnitine treatment attenuates renal tubulointerstitial fibrosis induced by unilateral ureteral obstruction
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Zhao Hai Yan
Li Hui Ying
Jin Jian
Jin Ji Zhe
Zhang Long Ye
Xuan Mei Ying
Jin Xue Mei
Jiang Yu Ji
Zheng Hai Lan
Jin Ying Shun
Jin Yong Jie
Choi Bum-Soon
Yang Chul-Woo
Piao Shang Guo
Li Can
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Abstract
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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.
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KEYWORD
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L-carnitine, Unilateral ureteral obstruction, Oxidative stress, Autophagy, Mitochondria
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