Abstract
BackgroundEarly 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.MethodsSevere 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.ResultsRenal 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.ConclusionHydrogen 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.
Highlights
Acute kidney injury (AKI) in severely burned patients predicts a high mortality that is multi-fac‐ torial
Acute kidney injury (AKI) is a devastating complication that affects patients exposed to severe burn injury [total body surface area (TBSA) ≥20%], which has been associated with a high mortality rate [1, 2]
Mitogen-activated protein kinases (MAPKs), including p38 MAPK, c-Jun N-terminal kinase (JNK), and extracellular signal-regulated kinase (ERK), play important roles in the mediation of apoptosis, cellular proliferation and differentiation, and previous studies have verified that MAPKs are involved in the pathogenesis and protection against acute kidney injury (AKI) caused by different stimuli [10]
Summary
Acute kidney injury (AKI) in severely burned patients predicts a high mortality that is multi-fac‐ torial. 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. AKI may be Combined with the apoptotic pathway, reactive oxygen species (ROS)-induced oxidative stress is involved in the development of renal dysfunction followed by AKI or other diseases [6, 7]. Mitogen-activated protein kinases (MAPKs), including p38 MAPK, c-Jun N-terminal kinase (JNK), and extracellular signal-regulated kinase (ERK), play important roles in the mediation of apoptosis, cellular proliferation and differentiation, and previous studies have verified that MAPKs are involved in the pathogenesis and protection against AKI caused by different stimuli [10]. ROS have been reported to be involved in MAPK activation [11, 12]
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