Protective role of H2S on acute renal damages in urinary-derived sepsis

• Main Authors: Wujun Xu, Yachun Tang, Xiaofeng Zhao, Liwen Zhao, Xiaobin Wu, Li Liu, Xiangyang Long, Zhigang Luo, Xian Chen, Binhui Wang
• Format: Article
• Language: English
• Published: Taylor & Francis Group 2019-01-01
• Series: Biotechnology & Biotechnological Equipment
• Subjects: h2s; urinary-derived sepsis; acute renal damages; inos; ho-1
• Online Access: http://dx.doi.org/10.1080/13102818.2019.1664929

The aim of this study was to investigate the protective roles of H2S on acute renal damage in urinary-derived sepsis. Totally 40 male rabbits were randomly divided into the Control, Sham, Sepsis, NaHS and the dl-propargylglycine (PAG) groups. White blood cell counts (WBC), C-reactive protein (CRP), creatinine (Cr) and blood urea nitrogen were determined in peripheral blood samples. Hematoxylin and eosin staining was performed to detect the morphological changes. The mRNA and protein expression levels were detected by semi-quantitative reverse transcriptase PCR (sqRT-PCR) and Western blot analysis. The results showed that, 72 h after surgery, the WBC and CRP levels in the Sepsis group were significantly elevated, and the expression levels of inducible nitric oxide synthase (iNOS) and HO-1 were significantly up-regulated, compared with the Control and Sham groups, indicating renal damage induced by urinary-derived sepsis. Compared with the Sepsis group, the expression levels of iNOS in the renal tissues of the PAG group were significantly up-regulated, whereas the expression levels of HO-1 in the renal tissue were significantly down-regulated, indicating aggravated renal damage. On the other hand, compared with the Sepsis group, the expression levels of iNOS in the renal tissue of the NaHS group were declined, whereas the expression levels of HO-1 were elevated, together with the declined WBC and CRP levels, indicating alleviated renal functions. We could conclude that iNOS and HO-1 expression levels are elevated in the renal tissue of urinary-derived sepsis. H2S could exert protective effects on the urinary-derived sepsis-associated renal damages by down-regulating iNOS expression and up-regulating HO-1 expression.