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2015 ; 8
(3
): 2680-9
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Inhalation of hydrogen gas ameliorates glyoxylate-induced calcium oxalate
deposition and renal oxidative stress in mice
#MMPMID26045773
Peng Z
; Chen W
; Wang L
; Ye Z
; Gao S
; Sun X
; Guo Z
Int J Clin Exp Pathol
2015[]; 8
(3
): 2680-9
PMID26045773
show ga
The aim of this study is to evaluate the protective effect and underlying
mechanism of hydrogen gas (H2) to glyoxylate induced renal calcium oxalate (CaOx)
crystal deposition in mice. In present work, rodent renal CaOx crystal deposition
model was introduced by intra-abdominal injection of glyoxylate (100 mg/kg/d) for
5 days. Two days before administration of glyoxylate, inhalation of H2 for 30 min
per day was initiated and continued for 7 days. By the end of the study, the
samples of 24 hours urine, serum and renal tissue were collected for biochemical
and pathological assay. According to levels of urine calcium excretion, renal
calcium deposition, a serum excretion of kidney injury molecule-1 (KIM-1) assay
and a TUNEL assay, inhalation of H2 could successfully decrease the CaOx
crystallizations and protect against renal injury. Crystal deposition in the
kidneys is associated with oxidative stress, which was indicated by increased
levels of renal malondialdehyde (MDA) and 8-hydroxydeoxyguanosine (8-OHdG) and
decreased activities of superoxide dismutase (SOD), glutathione (GSH) and
catalase (CAT). These effects were reversed by a high-dose H2 pretreatment. The
renal expressions of osteopontin (OPN), CD44, monocyte chemoattractant protein-1
(MCP-1) and interleukin-10 (IL-10) were markedly increased in glyoxylate-treated
mice, and H2 significantly attenuated the increase of OPN, CD44 and MCP-1 but
upregulated the expression of IL-10. Our findings demonstrate that inhalation of
H2 reduces renal crystallization, renal oxidative injury and inflammation and it
may be a candidate agent with few adverse effects for prevention of
nephrolithiasis.