Saturated hydrogen alleviates CCl-induced acute kidney injury via JAK2/STAT3/p65 signaling.

OBJECTIVES

This study assessed the protective effects of saturated hydrogen against CCl-induced acute kidney injury (AKI) in mice, and investigated signaling pathways activated by exposure to saturated hydrogen.

METHODS

A mouse model of CCl-induced AKI was established; some mice were treated with saturated hydrogen. Levels of cystatin C and kidney injury molecule 1 were determined using enzyme-linked immunosorbent assays. Blood urea nitrogen and serum creatinine were measured on a fully automated biochemical analyzer. Interleukin-8, tumor necrosis factor-α, and interferon-γ in serum and kidney tissues were measured using enzyme-linked immunosorbent assays. Malondialdehyde, glutathione peroxidase, and superoxide dismutase in kidney tissues were measured using biochemical kits. Oxidative stress in kidney tissues was analyzed using nitrotyrosine staining. Expression levels of p-JAK2, p-STAT3, and p-p65 signal protein were assayed by immunohistochemistry and western blotting.

RESULTS

Compared with untreated mice with CCl-induced AKI, mice that were treated with saturated hydrogen exhibited improved renal function and reduced oxidative stress. Moreover, expression levels of p-JAK2, p-STAT3, and p-p65 were significantly reduced in mice treated with saturated hydrogen, compared with expression levels in untreated mice.

CONCLUSIONS

Treatment with saturated hydrogen can reduce oxidative stress and inflammatory cytokine activation, potentially through inhibition of JAK2/STAT3/p65 signaling, thereby protecting against AKI.