Dioscin relieves diabetic nephropathy <i>via</i> suppressing oxidative stress and apoptosis, and improving mitochondrial quality and quantity control
Yujie Zhong, Jiayu Liu, Dianjun Sun, Tianmin Guo, Yanpeng Yao, Xiaodong Xia, Chao Shi, Xiaoli Peng
Abstract
regulating Parkin, PINK1, DRP1, p-DRP1 and MFN2 expressions. Collectively, these results suggested that dioscin protected against DN through inhibiting oxidative stress, inflammation, and apoptosis mediated by the mitochondria and ER stress. Autophagy and mitochondrial quality and quantity control (mitophagy and mitochondrial fission/fusion) were also improved by dioscin.
Topics & Concepts
MitophagyMFN2PINK1Mitochondrial fissionAutophagyOxidative stressApoptosisPharmacologyMitochondrionDiabetic nephropathyChemistrymitochondrial fusionBiologyBiochemistryEndocrinologyKidneyMitochondrial DNAGeneAutophagy in Disease and TherapyAdvanced Glycation End Products researchEndoplasmic Reticulum Stress and Disease