Suppression of HDAC2 by sodium butyrate alleviates apoptosis of kidney cells in db/db mice and HG‑induced NRK‑52E cells

Butyrate is short‑chain fatty acid, which is produced by intestinal microbiota metabolizing dietary fibers. Butyrate participates in various physiological processes predominantly by activating G‑coupled‑receptors, inhibiting histone deacetylases (HDACs) and serving as an energy substrate. Previous s...

Full description

Saved in:
Bibliographic Details
Published inInternational journal of molecular medicine Vol. 45; no. 1; pp. 210 - 222
Main Authors Du, Yi, Tang, Gang, Yuan, Weijie
Format Journal Article
LanguageEnglish
Published Greece Spandidos Publications 01.01.2020
Spandidos Publications UK Ltd
D.A. Spandidos
Subjects
Antioxidants (Nutrients)
Apoptosis
Biotechnology industries
Diabetes
Diabetic nephropathies
Diabetic nephropathy
Esters
Fatty acids
Glucose
Inflammation
Kidney diseases
Laboratory animals
Messenger RNA
Microbiota
Microbiota (Symbiotic organisms)
Oxidative stress
Plasmids
RNA
Rodents
Scientific equipment industry
Studies
United States
Japan
Online AccessGet full text

Cover

More Information
Summary:Butyrate is short‑chain fatty acid, which is produced by intestinal microbiota metabolizing dietary fibers. Butyrate participates in various physiological processes predominantly by activating G‑coupled‑receptors, inhibiting histone deacetylases (HDACs) and serving as an energy substrate. Previous studies have shown that butyrate plays a protective role in diabetic nephropathy (DN); however, the exact mechanism remains unclear. The present study identified that providing sodium butyrate (NaBu) by gavage relieved renal damage and apoptosis in db/db mice, which is a widely used type 2 DN model. In vitro, NaBu suppressed high glucose (HG)‑induced apoptosis in normal rat kidney tubular epithelial (NRK‑52E) cells. Of the eleven HDACs (HDAC1‑11) studied, only the mRNA expression of HDAC2 was attenuated by NaBu in NRK‑52E cells under the HG condition. Overexpression of HDAC2 offset the anti‑apoptotic effect of NaBu. NaBu also suppressed HG‑induced oxidative stress. Additionally, H2O2 induced an upregulation of HDAC2 in NRK‑52E cells, while NaBu inhibited this process. Mechanistically, NaBu acted as an antioxidant in HG‑induced NRK‑52E cells and suppressed HG‑induced apoptosis of NRK‑52E cells through inhibiting HDAC2 by virtue of its anti‑oxidative property.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 14
ISSN:1107-3756
1791-244X
DOI:10.3892/ijmm.2019.4397