Inhalation of Hydrogen Gas Is Beneficial for Preventing Contrast-Induced Acute Kidney Injury in Rats

Homma, Koichiro; Yoshida, Tadashi; Yamashita, Mitsuaki; Hayashida, Kei; Hayashi, Matsuhiko; Hori, Shingo

doi:10.1159/000369068

Cited by 21 publications

(21 citation statements)

References 25 publications

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“…We also observed tubular epithelial necrosis by microscopic detection, similar to other studies on AKI caused by different reasons [31–33]. Applied HS, less necrotic tubules were found with a lower tubular damage score, which suggests a relief of early AKI post burn.…”

Section: Discussionsupporting

confidence: 89%

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

et al. 2015

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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.

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Section: Discussionsupporting

confidence: 89%

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

et al. 2015

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“…Proteinaceous casts, tubular necrosis, and medullary congestion are established histologic features of ischemic AKI. 1,2,18,19 Histologic analyses revealed that Klf4 deletion significantly exacerbated the formation of proteinaceous casts and tubular necrosis and the degree of medullary congestion in response to I/R injury ( Figure 3). These results suggest that endothelial Klf4 plays a protective role in ischemic AKI.…”

Section: Endothelial Klf4 Deletion Exacerbated Renal I/r Injurymentioning

confidence: 99%

“…Histologic analyses were performed, as previously described. 18 Immunohistochemistry was performed with antibodies for Klf4, 36 neutrophil (7/4; Abcam, Inc., Cambridge, MA), CD3« (M20; Santa Cruz Biotechnology, Santa Cruz, CA), Ly6c (ER-MP20; Abcam, Inc.), and F4/80 (CI:A3-1; Abcam, Inc.). Staining was visualized by diaminobenzidine, and sections were counterstained by hematoxylin.…”

Section: Histology and Immunohistochemistrymentioning

confidence: 99%

Endothelial Krüppel-Like Factor 4 Mediates the Protective Effect of Statins against Ischemic AKI

Yoshida

Yamashita

Iwai

et al. 2015

JASN

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Endothelial cells participate in the pathophysiology of ischemic AKI by increasing the expression of cell adhesion molecules and by recruiting inflammatory cells. We previously showed that endothelial Krüppel-like factor 4 (Klf4) regulates vascular cell adhesion molecule 1 (Vcam1) expression and neointimal formation after carotid injury. In this study, we determined whether endothelial Klf4 is involved in ischemic AKI using endothelial Klf4 conditional knockout (Klf4 cKO) mice generated by breeding Tek-Cre mice and Klf4 floxed mice. Klf4 cKO mice were phenotypically normal before surgery. However, after renal ischemia-reperfusion injury, Klf4 cKO mice exhibited elevated serum levels of urea nitrogen and creatinine and aggravated renal histology compared with those of Klf4 floxed controls. Moreover, Klf4 cKO mice exhibited enhanced accumulation of neutrophils and lymphocytes and elevated expression of cell adhesion molecules, including Vcam1 and Icam1, in injured kidneys. Notably, statins ameliorated renal ischemia-reperfusion injury in control mice but not in Klf4 cKO mice. Mechanistic analyses in cultured endothelial cells revealed that statins increased KLF4 expression and that KLF4 mediated the suppressive effect of statins on TNFa-induced VCAM1 expression by reducing NF-kB binding to the VCAM1 promoter. These results provide evidence that endothelial Klf4 is renoprotective and mediates statin-induced protection against ischemic AKI by regulating the expression of cell adhesion molecules and concomitant recruitment of inflammatory cells.

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“…Thus, we recently created contrast medium model rats and reported on our investigation of the effectiveness of hydrogen gas inhalation as a preventative for CIAKI. 53 Specifically, we investigated the effect on renal function and renal tissue of hydrogen gas inhalation by rats on administration of contrast medium, as compared to rats who inhaled a control gas. The results indicated that the inhalation of hydrogen gas suppressed the decrease in renal function caused by the administration of contrast medium.…”

Section: Future Directionsmentioning

confidence: 99%

Contrast-induced Acute Kidney Injury

Homma

2016

Keio J. Med.

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Because of the increased use of contrast media, the potential risk of contrast-induced acute kidney injury (CIAKI) has also increased. CIAKI often results in chronic kidney disease (CKD), an affliction with increasing incidence in modern society. The current prevalence of CIAKI is difficult to estimate because most victims are asymptomatic. The first Japanese guidelines regarding contrast agent examinations were recently announced, but their only recommendation is to provide classic fluid replacement with saline 6-12 h before and after the contrast procedure. According to a review summarizing the recent literature, little evidence supports this suggestion. To obtain early diagnoses and to treat emergent patients, it is appropriate to perform procedures using contrast media without knowledge of patients' renal function. Prevention of CIAKI is the most important consideration, and the usefulness of risk scores predicting the development of CIAKI has been reported. However, no prospective studies have been performed to date, and, therefore, such studies will be necessary in the future. Furthermore, the development of novel preventative interventions for CIAKI is also required.

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Inhalation of Hydrogen Gas Is Beneficial for Preventing Contrast-Induced Acute Kidney Injury in Rats

Cited by 21 publications

References 25 publications

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

Endothelial Krüppel-Like Factor 4 Mediates the Protective Effect of Statins against Ischemic AKI

Contrast-induced Acute Kidney Injury

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