Effects of hydrogen-rich saline on early acute kidney injury in severely burned rats by suppressing oxidative stress induced apoptosis and inflammation.
Effects of hydrogen-rich saline on early acute kidney injury in severely burned rats by suppressing oxidative stress induced apoptosis and inflammation.
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富氢盐水通过抑制氧化应激诱导的细胞凋亡和炎症对严重烧伤大鼠早期急性肾损伤的影响
DOI:
10.1186/s12967-015-0548-3
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发表时间:
2015-06-06
影响因子:
7.4
通讯作者:
Han CM
中科院分区:
文献类型:
--
作者:
Guo SX;Fang Q;You CG;Jin YY;Wang XG;Hu XL;Han CM
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.
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影响因子:
3.7
作者:
Guo SX;Jin YY;Fang Q;You CG;Wang XG;Hu XL;Han CM
通讯作者:
Han CM
DOI:
10.1155/2011/768512
发表时间:
2011
期刊:
Journal of signal transduction
影响因子:
--
作者:
Feliers D;Kasinath BS
通讯作者:
Kasinath BS
DOI:
10.1016/j.bbrc.2008.05.165
发表时间:
2008-08-15
影响因子:
3.1
作者:
Hayashida, Kentaro;Sano, Motoaki;Fukuda, Keiichi
通讯作者:
Fukuda, Keiichi
DOI:
10.1016/j.bbrc.2007.07.088
发表时间:
2007-09-28
影响因子:
3.1
作者:
Fukuda, Kei-Ichi;Asoh, Sadamitsu;Ohta, Shigeo
通讯作者:
Ohta, Shigeo
影响因子:
3.8
作者:
Hoesel, Laszlo M.;Mattar, Aladdein F.;Hemmila, Mark R.
通讯作者:
Hemmila, Mark R.