| 저자 |
Dae-Hong Jeon, Jin Hyun Kim, Ha Nee Jang, Min Jeong Kim, Hyun Seop Cho, Hyun-Jung Kim, Se-Ho Chang, Dong Jun Park |
| 초록 |
Introduction and Aims: Although hydrogen sulfide (H2S), the third endogenous gaseous molecule with important physiological roles, is beneficial in chronic kidney disease, the role of H2S in acute kidney injury (AKI) remains to be controversial. The present study aimed to investigate the effect of H2S on cisplatin (CP)-induced AKI in mice by administrating exogenous H2S.
Methods: Mice were randomly divided into control group, sodium hydrosulfide (NaHS) only group (NaHS 56 μmol/kg, i.p., day -1 through day 3), CP group (20mg/kg, i.p., day 0), CP+NaHS groups, with 10 mice in each group. Blood sample was collected 3 day after cisplatin for renal function and enzyme activity and the kidneys were harvested for histological, immunohistochemical and Western blot analysis. Cystathionine-γ-lyase (CSE) activity was measured by the spectrophotometric methylene blue method.
Results: CP-treated mice demonstrated increases in serum creatinine and blood urea nitrogen (BUN). NaHS administration prevented this deterioration of renal function. The pathological features of kidney injury were also alleviated by NaHS. The H2S concentration was significantly decreased in the cisplatin group and this reduction was attenuated by the NaHS treatment. In the CP-treated mice, the levels of CSE, nuclear factor κ-light-chain-enhancer of activated B cells (NF-κB), MAPKs, and pSmad were significantly increased. All these alterations were reduced by treatment of NaHS whereas cystathionine β-synthase (CBS) level was significantly increased.
Conclusions: Treatment with NaHS attenuates CP-induced AKI in the mice resulting in elevation of CSE and decrease of CBS. This effect seems to be involved with the restriction of the inflammation in the kidneys from NaHS+CP-treated mice. Therefore, hydrogen sulfide might have therapeutic potentials in preventing AKI in conditions to receive CP. |