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The aim of the present study was to investigate the effects of endogenous H 2 S on the inflammatory response in kidneys following urine-derived sepsis-induced injury. A rabbit model of urine-derived sepsis was established by injecting Escherichia coli into the ligated ureter. Rabbits were randomly divided into the, control, sham, sepsis and DL-propargylglycine (PAG)-treated sepsis groups. The same surgical procedure except for the bacteria injection was performed for the sham group, while the control group was fed on normal diet without any additional treatments. The monitoring of vital signs, routine blood examinations and kidney function tests were performed prior to surgery and at 12, 24, 36 and 48 h following surgery. The serum H 2 S concentration and kidney cystathionine-γ-lyase (CSE) activity were determined following surgery. Pathological alterations were assessed by hematoxylin and eosin (H&amp;E) staining, and the expression levels of inflammation-associated cytokines were detected by western blot analysis. The results demonstrated that rabbits in the sepsis and PAG groups exhibited a significant increase in rectal temperature, heart rate and respiratory rate following surgery when compared with the sham group; with the PAG group demonstrating the greatest increase. In addition, white cell counts and creatinine and urea nitrogen levels were significantly elevated following surgery in the sepsis and PAG groups when compared with the sham group. The serum H 2 S concentration and kidney CSE activity were significantly reduced in the sepsis group compared with the sham group, and a significant decrease in the levels of these factors were observed in the PAG group compared with the sepsis group. H&amp;E staining indicated obvious structural abnormalities in kidney tissues in the sepsis group, which were exacerbated by PAG treatment. In addition, PAG treatment significantly increased the expression levels of nuclear factor-κB and interleukin-6, and decreased transforming growth factor-β1 expression when compared with the sepsis group. In conclusion, PAG significantly exacerbated urine-derived sepsis-induced kidney injury potentially via altering the expression of inflammation-associated cytokines.

Inhibition of endogenous hydrogen sulfide production exacerbates the inflammatory response during urine‑derived sepsis‑induced kidney injury