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Mol Med Rep 12: 4291-4297, 2015; DOI: 10.3892/mmr.2015.3964 Subsequently to the publication of the above paper, an interested reader has drawn to the authors' attention that, in Fig. Immunostaining for (A-D) OPN and (E-H) CD44 in tissue samples from rat kidneys. [Extracted from the article]

Subsequently to the publication of the above paper, an interested reader has drawn to the authors' attention that, in Fig. 4, there appeared to be an overlap between the data shown in the 4B (OPN/saline) and the 4C (OPN/DMSO) panels, such that these data may have been derived from the same original source even though different experimental conditions were described in the Figure; furthermore, the Fig. 4F (saline) and 4G (DMSO) panels appeared to be very similar, as if they were tissue sections from the same specimen. Upon examining the final proofs of this article, the authors have determined that the immunohistochemical images of the saline groups were incorrectly selected. A further examination of the original data files disclosed that an error had been made in the labelling of some of the original images. The corrected version of Fig. 4, including the correct data for Fig. 4B and F (for the immunostaining of OPN and CD44, respectively, under saline conditions), is shown opposite. Note that these errors did not affect either the results or the conclusions reported in this paper, and all the authors agree to this Corrigendum. The authors are grateful to the Editor of Molecular Medicine Reports for allowing them the opportunity to publish this Corrigendum, and apologize to the readership for any inconvenience caused. [the original article was published in Molecular Medicine Reports 12: 4291-4297, 2015; DOI: 10.3892/mmr.2015.3964].

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.