4.7 Article

A natural product of acteoside ameliorate kidney injury in diabetes db/db mice and HK-2 cells via regulating NADPH/oxidase-TGF-β/Smad signaling pathway

Journal

PHYTOTHERAPY RESEARCH
Volume 35, Issue 9, Pages 5227-5240

Publisher

WILEY
DOI: 10.1002/ptr.7196

Keywords

acteoside; diabetic kidney disease; metabolic profiling; NADPH/oxidase-TGF-beta/Smad signaling pathway; ROS

Funding

  1. National Natural Science Foundation of China [8197141957, 81373889, 81673533]
  2. Priority Academic Program Development of Jiangsu Higher Education Institutions [ysxk-2014]

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The study found that acteoside exhibited renal protective effects by inhibiting specific signaling pathways in diabetes mice and high glucose-induced cells, regulating metabolic pathways. This research provides important insights for further exploring the pathogenesis and development of therapeutic agents for diabetic kidney disease.
This study was designed to investigate the protective effects and mechanisms of acteoside on DKD in diabetes male db/db mice and high glucose-induced HK-2 cells. The diabetes db/db mice were divided randomly into model group, metformin group, irbesartan group, and acteoside group. We observed the natural product of acteoside exhibiting a significant effect in renal protection through analyzing of biochemical indicators and endogenous metabolites, histopathological observations, and western blotting. HK-2 cells subjected to high glucose were used in invitro experiments. The molecular mechanisms of them were investigated by RT-PCR and western blot. Acteoside prevents high glucose-induced HK-2 cells and diabetes db/db mice by inhibiting NADPH/oxidase-TGF-beta/Smad signaling pathway. Acteoside regulated the disturbed metabolic pathway of lipid metabolism, glyoxylate and dicarboxylate metabolism, and arachidonic acid metabolism. We discovered the natural product of acteoside exhibiting a significant effect in renal protection. This study paved the way for further exploration of pathogenesis, early diagnosis, and development of a new therapeutic agent for DKD.

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