ArticleInternational journal of molecular medicine2020
Suppression of HDAC2 by sodium butyrate alleviates apoptosis of kidney cells in db/db mice and HG‑induced NRK‑52E cells.
Article in International journal of molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 42 citations in OpenAlex.
- Sodium butyrate induces apoptosis enhanced by JAK2 inhibitor Fedratinib in NK/T-cell lymphoma cell.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Article
- Microbial short chain fatty acids: Effective histone deacetylase inhibitors in immune regulation (Review).International journal of molecular medicine · 2026Review
- Histone deacetylases and their inhibitors in kidney diseases.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- Review
- Sodium butyrate inhibits activation of ROS/NF-κB/NLRP3 signaling pathway and angiogenesis in human retinal microvascular endothelial cells.International ophthalmology · 2025Article
- Beneficial Effects of Butyrate on Kidney Disease.Nutrients · 2025Review
- Long noncoding RNA Gm4419 promotes mesangial cell proliferation and extracellular matrix accumulationHeliyon · 2025Article
- Gut microbiota-derived SCFAs and MetS-related nephropathy.Frontiers in nutrition · 2025Review
- Oxidative stress and its related epigenetic modifications in vascular calcification: mechanisms and advances.Frontiers in cardiovascular medicine · 2025Review
- Acetylation in renal physiology and pathophysiology.Frontiers in pharmacology · 2025Review
- Sodium butyrate ameliorates high glucose-suppressed neuronal mitophagy by restoring PRKN expression via inhibiting the RELA-HDAC8 complex.Autophagy · 2024Article
- Kidney Aging and Chronic Kidney Disease.International journal of molecular sciences · 2024Review
- The potential mechanism of gut microbiota-microbial metabolites-mitochondrial axis in progression of diabetic kidney disease.Molecular medicine (Cambridge, Mass.) · 2023Review
- Specific gut microbiome and metabolome changes in patients with continuous ambulatory peritoneal dialysis and comparison between patients with different dialysis vintages.Frontiers in medicine · 2023Article
- Intestinal microbiota dysbiosis in acute kidney injury: novel insights into mechanisms and promising therapeutic strategies.Renal failure · 2022Review
- Gut Microbiota Mediates the Protective Effects of Traditional Chinese Medicine Formula Qiong-Yu-Gao against Cisplatin-Induced Acute Kidney Injury.Microbiology spectrum · 2022Article
- Changes of gut microbiota in diabetic nephropathy and its effect on the progression of kidney injury.Endocrine · 2022Article
- Efficacy of probiotics on the modulation of gut microbiota in the treatment of diabetic nephropathy.World journal of diabetes · 2022Review
- The role and mechanism of butyrate in the prevention and treatment of diabetic kidney disease.Frontiers in microbiology · 2022Review
- Inhibition of HDAC6 With CAY10603 Ameliorates Diabetic Kidney Disease by Suppressing NLRP3 Inflammasome.Frontiers in pharmacology · 2022Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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