Open Access

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

  • Authors:
    • Huili Qiu
    • Xian Chen
    • Zhigang Luo
    • Liwen Zhao
    • Tao Zhang
    • Ning Yang
    • Xiangyang Long
    • Huang Xie
    • Jun Liu
    • Wujun Xu
  • View Affiliations

  • Published online on: July 25, 2018     https://doi.org/10.3892/etm.2018.6520
  • Pages: 2851-2858
  • Copyright: © Qiu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

The aim of the present study was to investigate the effects of endogenous H2S 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 H2S concentration and kidney cystathionine‑γ‑lyase (CSE) activity were determined following surgery. Pathological alterations were assessed by hematoxylin and eosin (H&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 H2S 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&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.
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October-2018
Volume 16 Issue 4

Print ISSN: 1792-0981
Online ISSN:1792-1015

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Spandidos Publications style
Qiu H, Chen X, Luo Z, Zhao L, Zhang T, Yang N, Long X, Xie H, Liu J, Xu W, Xu W, et al: Inhibition of endogenous hydrogen sulfide production exacerbates the inflammatory response during urine‑derived sepsis‑induced kidney injury. Exp Ther Med 16: 2851-2858, 2018
APA
Qiu, H., Chen, X., Luo, Z., Zhao, L., Zhang, T., Yang, N. ... Xu, W. (2018). Inhibition of endogenous hydrogen sulfide production exacerbates the inflammatory response during urine‑derived sepsis‑induced kidney injury. Experimental and Therapeutic Medicine, 16, 2851-2858. https://doi.org/10.3892/etm.2018.6520
MLA
Qiu, H., Chen, X., Luo, Z., Zhao, L., Zhang, T., Yang, N., Long, X., Xie, H., Liu, J., Xu, W."Inhibition of endogenous hydrogen sulfide production exacerbates the inflammatory response during urine‑derived sepsis‑induced kidney injury". Experimental and Therapeutic Medicine 16.4 (2018): 2851-2858.
Chicago
Qiu, H., Chen, X., Luo, Z., Zhao, L., Zhang, T., Yang, N., Long, X., Xie, H., Liu, J., Xu, W."Inhibition of endogenous hydrogen sulfide production exacerbates the inflammatory response during urine‑derived sepsis‑induced kidney injury". Experimental and Therapeutic Medicine 16, no. 4 (2018): 2851-2858. https://doi.org/10.3892/etm.2018.6520