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Biochem Biophys Res Commun. 2014 May 16;447(4):666-71. doi: 10.1016/j.bbrc.2014.04.074. Epub 2014 Apr 19.

Protective effects of exogenous β-hydroxybutyrate on paraquat toxicity in rat kidney.

Author information

1
College of Veterinary Medicine, Jilin University, China.
2
College of Veterinary Medicine, Jilin University, China. Electronic address: xiegh@jlu.edu.cn.

Abstract

In this study, we demonstrated the protective effects of β-hydroxybutyrate (β-HB) against paraquat (PQ)-induced kidney injury and elucidated the underlying molecular mechanisms. By histological examination and renal dysfunction specific markers (serum BUN and creatinine) assay, β-HB could protect the PQ-induced kidney injury in rat. PQ-induced kidney injury is associated with oxidative stress, which was measured by increased lipid peroxidation (MDA) and decreased intracellular anti-oxidative abilities (SOD, CAT and GSH). β-HB pretreatment significantly attenuated that. Caspase-mediated apoptosis pathway contributed importantly to PQ toxicity, as revealed by the activation of caspase-9/-3, cleavage of PARP, and regulation of Bcl-2 and Bax, which were also effectively blocked by β-HB. Moreover, treatment of PQ strongly decreased the nuclear Nrf2 levels. However, pre-treatment with β-HB effectively suppressed this action of PQ. This may imply the important role of β-HB on Nrf2 pathway. Taken together, this study provides a novel finding that β-HB has a renoprotective ability against paraquat-induced kidney injury.

KEYWORDS:

Apoptosis; Kidney injury; Oxidative stress; Paraquat; β-Hydroxybutyrate

PMID:
24755084
DOI:
10.1016/j.bbrc.2014.04.074
[Indexed for MEDLINE]

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