Abstract: [Abstract] Objective    to investigate the effect and mechanism of hydrogen sulfide (H2S) on kidney injury induced by urinary-derived sepsis. Methods   Rabbits were randomly divided into control group, sham group, sepsis group, NaHS 2.8 umol/kg group, and NaHS 8.4 umol/kg group, with 6 rabbits in each group. Upper urinary tract obstruction and acute infection was induced to establish sepsis model. Blood was taken for white blood cell count (WBC), creatinine (Cr) and blood urea nitrogen (BUN) analysis. Morphological changes were observed by HE staining and transmission electron microscopy. Immunohistochemical staining was used to detect TNF-α, IL-10 and NF-κB expression. Cystathionine-γ-lyase (CSE) activity was measured by spectrophotometric methylene blue method and blood H2S concentration by deproteinization. Results   Levels of WBC, Cr and BUN were significantly elevated in sepsis group than control group (P < 0.05). After treatment with NaHS, levels of WBC, Cr and BUN were significantly decreased in NaHS groups than sepsis group (P < 0.05). And pathological features of kidney injury were also alleviated by NaHS. In sepsis group, levels of TNF-α, IL-10 and NF-κB were significantly increased (P < 0.05). In NaHS groups, TNF-α and NF-κB levels were significantly inhibited whereas IL-10 level was significantly increased (P < 0.05). H2S content was significantly decreased in sepsis group whereas significantly increased in NaHS group (P < 0.05). Additionally, NaHS 8.4 umol/kg group had better effect than NaHS 2.8umol/kg group. Conclusion   Exogenous H2S reduced kidney injury of urinary-derived sepsis by inhibiting NF-κB, decreasing TNF-α and increasing IL-10.

Key words: hydrogen sulfide, NF-kappa B, tumor necrosis factor-alpha, interleukin-10, cystathionine gamma-ly?ase, kidney injury, urinary-derived sepsis