Hispidulin alleviates high-glucose-induced podocyte injury by regulating protective autophagy

Biomedicine & Pharmacotherapy = Biomédecine & Pharmacothérapie
Fengbo WuBo Han

Abstract

Diabetic nephropathy (DN) is one of the most common complications in patients with diabetes, and the discovery of novel targeted therapeutic approaches for DN treatment still faces severe challenges. In the current study, we aimed to discover a novel natural product for potential DN treatment and determine its molecular mechanisms. Methylthiazoltetrazolium (MTT) assay was employed to evaluate cell viability. Transmission electron microscopy, GFP-LC3 fluorescence fusion plasmid, and Annexin V/PI apoptosis assay were carried out to determine cellular autophagy and apoptosis. Moreover, quantitative proteomics and bioinformatics analysis, Western blotting, and RNA interference were performed to investigate potential molecular mechanisms. Hispidulin displayed protective capacity on the high-glucose-induced podocyte injury models by activating autophagy and inhibiting apoptosis. The mechanism for hispidulin-induced autophagy was associated to Pim1 inhibition and the regulation of Pim1-p21-mTOR signaling axis. Moreover, quantitative proteomics and bioinformatics analysis revealed that the hispidulin-regulated Pim1 inhibition was associated to RAB18, NRas, PARK7, and FIS1. These results indicate that hispidulin induces autophagy and in...Continue Reading

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Citations

Sep 20, 2019·Journal of Diabetes Research·Zhenzhen LuYueyi Deng
Dec 13, 2019·Journal of Diabetes Research·Yuyang WangPing Li
Jul 23, 2020·Journal of Diabetes Research·Dorin DragoșDorin Ionescu
Jul 2, 2020·Diabetes, Metabolic Syndrome and Obesity : Targets and Therapy·Caigu HeYanfang Zheng
Jan 29, 2021·Food and Chemical Toxicology : an International Journal Published for the British Industrial Biological Research Association·Xuliang ZhangYanfei Li
Apr 13, 2021·Frontiers in Endocrinology·Ugochukwu Kelvin IhenachoR Blake Hill
Sep 22, 2021·Antioxidants & Redox Signaling·Alaa Abou DaherAssaad A Eid

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