Effects of hydrogen-rich saline on early acute kidney injury in severely burned rats by suppressing oxidative stress induced apoptosis and inflammation

• Published in: Journal of translational medicine 2015-06, Vol.13 (1), p.183-183, Article 183
• Main Authors: Guo, Song-Xue, Fang, Quan, You, Chuan-Gang, Jin, Yun-Yun, Wang, Xin-Gang, Hu, Xin-Lei, Han, Chun-Mao
• Format: Article
• Language: English
• Subjects: Acute Kidney Injury - blood; Acute Kidney Injury - complications; Acute Kidney Injury - drug therapy; Acute Kidney Injury - pathology; Acute-Phase Proteins; Analysis; Animals; Antioxidants; Apoptosis; Apoptosis - drug effects; Blotting, Western; Burns - blood; Burns - complications; Burns - drug therapy; Burns - pathology; Creatinine - blood; Enzyme-linked immunosorbent assay; Enzymes; Health aspects; Hydrogen; Hydrogen - pharmacology; Hydrogen - therapeutic use; Immunohistochemistry; Inflammation; Inflammation - complications; Inflammation - pathology; Inflammation Mediators - metabolism; Kidney Tubules - drug effects; Kidney Tubules - pathology; Lipocalins - blood; Male; Mediation; Medical research; Medicine, Experimental; Models, Biological; Oxidative stress; Oxidative Stress - drug effects; Peroxidase - metabolism; Prognosis; Proto-Oncogene Proteins - blood; Rats, Sprague-Dawley; Real-Time Polymerase Chain Reaction; Signal Transduction - drug effects; Sodium Chloride - pharmacology; Sodium Chloride - therapeutic use
• ISSN: 1479-5876; 1479-5876
• DOI: 10.1186/s12967-015-0548-3

Early acute kidney injury (AKI) in severely burned patients predicts a high mortality that is multi-factorial. Hydrogen has been reported to alleviate organ injury via selective quenching of reactive oxygen species. This study investigated the potential protective effects of hydrogen against severe burn-induced early AKI in rats. Severe burn were induced via immersing the shaved back of rats into a 100°C bath for 15 s. Fifty-six Sprague-Dawley rats were randomly divided into Sham, Burn + saline, and Burn + hydrogen-rich saline (HS) groups, and renal function and the apoptotic index were measured. Kidney histopathology and immunofluorescence staining, quantitative real-time PCR, ELISA and western blotting were performed on the sera or renal tissues of burned rats to explore the underlying effects and mechanisms at varying time points post burn. Renal function and tubular apoptosis were improved by HS treatment. In addition, the oxidation-reduction potential and malondialdehyde levels were markedly reduced with HS treatment, whereas endogenous antioxidant enzyme activities were significantly increased. HS also decreased the myeloperoxidase levels and influenced the release of inflammatory mediators in the sera and renal tissues of the burned rats. The regulatory effects of HS included the inhibition of p38, JNK, ERK and NF-κB activation, and an increase in Akt phosphorylation. Hydrogen can attenuate severe burn-induced early AKI; the mechanisms of protection include the inhibition of oxidative stress induced apoptosis and inflammation, which may be mediated by regulation of the MAPKs, Akt and NF-κB signalling pathways.