Open Access

Vorinostat protects against calcium oxalate-induced kidney injury in mice

Corrigendum in: /10.3892/mmr.2020.11782

  • Authors:
    • Li Wang
    • Wei Chen
    • Zhongjiang Peng
    • Changcheng Liu
    • Caihong Zhang
    • Zhiyong Guo
  • View Affiliations

  • Published online on: June 19, 2015     https://doi.org/10.3892/mmr.2015.3964
  • Pages: 4291-4297
  • Copyright: © Wang et al. This is an open access article distributed under the terms of Creative Commons Attribution License [CC BY_NC 3.0].

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Abstract

The present study aimed to examine the effect of the histone deacetylase inhibitor, vorinostat (SAHA), on renal function in a calcium oxalate crystal mouse model, and to investigate the mechanism underlying the renoprotective effect of SAHA. Calcium oxalate crystal formation was induced in 8 week‑old male C57BL/6 mice by administering 100 mg/kg glyoxylate for 7 days. A total of 24 male C57BL/6 mice were randomly divided into a control group and the following experimental groups: 50 mg/kg normal saline + 100 mg/kg glyoxylate; 50 mg/kg dimethyl sulfoxide (DMSO) + 100 mg/kg glyoxylate; and 50 mg/kg SAHA + 100 mg/kg glyoxylate. The mice in each of the experimental groups were injected with the saline, DMSO or SAHA into their abdominal cavities 6 h prior to the glyoxylate injection. The mice were sacrificed after 7 days, following which blood and urine samples were collected. The kidneys were harvested to analyze the levels of calcium concentrations and the levels of malondialdehyde (MDA), superoxide dismutase and glutathione reductase. Immunohistochemical staining and semi‑quantitative analyses were performed to detect the expression levels of osteopontin (OPN) and CD44. Renal tubular cell apoptosis was detected using a TUNEL assay. The concentrations of calcium and malondialdehyde were significantly decreased in the SAHA group, and calcium oxalate crystals in the kidney tissue and the expression levels of OPN and CD44 in the SAHA group were lower, compared with the other experimental groups. SAHA significantly reduced the urinary excretion of KIM‑1 and renal tubular cell apoptosis. In conclusion, SAHA reduced calcium oxalate crystal deposition and protected against kidney injury.
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September-2015
Volume 12 Issue 3

Print ISSN: 1791-2997
Online ISSN:1791-3004

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Spandidos Publications style
Wang L, Chen W, Peng Z, Liu C, Zhang C and Guo Z: Vorinostat protects against calcium oxalate-induced kidney injury in mice Corrigendum in /10.3892/mmr.2020.11782. Mol Med Rep 12: 4291-4297, 2015
APA
Wang, L., Chen, W., Peng, Z., Liu, C., Zhang, C., & Guo, Z. (2015). Vorinostat protects against calcium oxalate-induced kidney injury in mice Corrigendum in /10.3892/mmr.2020.11782. Molecular Medicine Reports, 12, 4291-4297. https://doi.org/10.3892/mmr.2015.3964
MLA
Wang, L., Chen, W., Peng, Z., Liu, C., Zhang, C., Guo, Z."Vorinostat protects against calcium oxalate-induced kidney injury in mice Corrigendum in /10.3892/mmr.2020.11782". Molecular Medicine Reports 12.3 (2015): 4291-4297.
Chicago
Wang, L., Chen, W., Peng, Z., Liu, C., Zhang, C., Guo, Z."Vorinostat protects against calcium oxalate-induced kidney injury in mice Corrigendum in /10.3892/mmr.2020.11782". Molecular Medicine Reports 12, no. 3 (2015): 4291-4297. https://doi.org/10.3892/mmr.2015.3964