Role of Parkin-mediated mitophagy in the protective effect of polydatin in sepsis-induced acute kidney injury

Journal of Translational Medicine
Youguang GaoBo Lin

Abstract

We have reported that polydatin (PD) alleviates mitochondrial dysfunction in rat models of sepsis-induced acute kidney injury (SI-AKI), but the mechanism is not well understood. Here, we investigated the role of Parkin-mediated mitophagy in the protective effects of PD in SI-AKI in mice. Sepsis was induced in the mice by caecal ligation and puncture. Mitophagy was determined by mitochondrial mass. NLRP3 inflammasome activation was determined by NLRP3, ASC and caspase-1. Mitophagy was blocked by treatment with mitochondrial division inhibitor-1 and Parkin knockout. PD treatment increased the sepsis-induced loss of mitochondrial mass, indicating the upregulation of mitophagy. Furthermore, PD treatment mediated Parkin translocation from the cytoplasm to the mitochondria. This suggests that Parkin-mediated mitophagy is an underlying mechanism. This was confirmed by the suppression of PD-induced mitophagy in Parkin-/- mice and in mice that were treated with a mitophagy inhibitor. PD-induced Parkin translocation and mitophagy were blocked by inhibiting SIRT1; thus, activation of SIRT1 might be an important molecular mechanism that is triggered by PD. Additionally, PD treatment protected against sepsis-induced kidney injury. These eff...Continue Reading

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Citations

May 22, 2020·FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology·Kehong ChenYani He
Nov 26, 2020·Nature Reviews. Nephrology·Chengyuan TangZheng Dong
Jan 27, 2021·Journal of Cellular and Molecular Medicine·Shao-Hua YuChi-Yuan Li
Apr 27, 2021·Biomedicine & Pharmacotherapy = Biomédecine & Pharmacothérapie·Zhicheng SunZhenchao Xu

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Methods Mentioned

BETA
density-gradient centrifugation
ELISA

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