Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2024 Oct;29(10):645-654.
doi: 10.1111/nep.14368. Epub 2024 Jul 29.

Hydrogen sulphide reduces renal ischemia-reperfusion injury by enhancing autophagy and reducing oxidative stress

Affiliations

Hydrogen sulphide reduces renal ischemia-reperfusion injury by enhancing autophagy and reducing oxidative stress

Hui Li et al. Nephrology (Carlton). 2024 Oct.

Abstract

Aim: Renal ischemia-reperfusion injury (IRI) is a major cause of acute kidney injury. Hydrogen sulphide (H2S) exerts a protective effect in renal IRI. The present study was carried out to investigate the effects of exogenous H2S on renal IRI by regulating autophagy in mice.

Methods: Mice were randomly assigned to control, IRI and NaHS (an H2S donor, 28, 56 and 100 μmol/kg) groups. Renal IRI was induced by clamping the bilateral renal pedicles with non-traumatic arterial clamp for 45 min and then reperfused for 24 h. Mice were administered intraperitoneally with NaHS 20 min prior to renal ischemia. Sham group mice underwent the same procedures without clamping. Serum and kidney tissues were harvested 24 h after reperfusion for functional, histological, oxidative stress, and autophagic determination.

Results: Compared with the control group, the concentrations of serum creatinine (Scr), blood urea nitrogen (BUN), and malondialdehyde (MDA), the protein levels of LC3II/I, Beclin-1 and P62, as well as the number of autophagosomes were significantly increased, but the activity of superoxide dismutase (SOD) was decreased after renal IRI. NaHS pre-treatment dramatically attenuated renal IRI-induced renal dysfunction, histological changes, MDA concentration and p62 expression in a dose-dependent manner. However, NaHS increased the SOD activity and the protein levels of LC3II/I and Beclin-1.

Conclusion: These results indicate that exogenous H2S protects the kidney from IRI through enhancement of autophagy and reduction of oxidative stress. Novel H2S donors could be developed in the treatment of renal IRI.

Keywords: autophagy; hydrogen sulphide; ischemia‐reperfusion injury; kidney.

PubMed Disclaimer

References

REFERENCES

    1. Eltzschig HK, Eckle T. Ischemia and reperfusion—from mechanism to translation. Nat Med. 2011;17(11):1391‐1401.
    1. Zhao HM, Qiu Y, Wu YC, Sun H, Gao S. Protective effects of GYY4137 on renal Ischaemia/reperfusion injury through Nrf2‐mediated antioxidant Defence. Kidney Blood Press Res. 2021;46(3):257‐265.
    1. Chertow GM, Burdick E, Honour M, Bonventre JV, Bates DW. Acute kidney injury, mortality, length of stay, and costs in hospitalized patients. J Am Soc Nephrol. 2005;16(11):3365‐3370.
    1. Mühlberger IM, Perco P, Fechete R, Mayer B, Oberbauer R. Biomarkers in renal transplantation ischemia reperfusion injury. Transplantation. 2009;88(3 Suppl):S14‐S19.
    1. Luo LN, Xie DQ, Zhang XG, Jiang R. Osthole decreases renal ischemia‐reperfusion injury by suppressing JAK2/STAT3 signaling activation. Exp Ther Med. 2016;12(4):2009‐2014.

MeSH terms

LinkOut - more resources