Beneficial Role of Hydrogen Sulfide in Renal Ischemia Reperfusion Injury in Rats.
10.3349/ymj.2018.59.8.960
- Author:
Eun Kyung CHOI
1
;
Sol Hee PARK
;
Jung A LIM
;
Seong Wook HONG
;
Kyung Hwa KWAK
;
Sung Sik PARK
;
Dong Gun LIM
;
Hoon JUNG
Author Information
1. Department of Anesthesiology and Pain Medicine, Yeungnam University College of Medicine, Daegu, Korea.
- Publication Type:Original Article
- Keywords:
Hydrogen sulfide;
ischemia-reperfusion injury;
cystathionine γ-lyase;
cystathionine β-synthase
- MeSH:
Animals;
Apoptosis;
Blood Urea Nitrogen;
Creatinine;
Cystathionine;
Cysteine;
Humans;
Hydrogen Sulfide*;
Hydrogen*;
Ischemia*;
JNK Mitogen-Activated Protein Kinases;
Kidney;
Male;
Malondialdehyde;
Oxidative Stress;
Phosphorylation;
Phosphotransferases;
Protein Kinases;
Rats*;
Rats, Sprague-Dawley;
Reperfusion;
Reperfusion Injury*;
Sodium;
Superoxide Dismutase;
Tissue Donors
- From:Yonsei Medical Journal
2018;59(8):960-967
- CountryRepublic of Korea
- Language:English
-
Abstract:
PURPOSE: Hydrogen sulfide (H2S) is an endogenous gaseous molecule with important physiological roles. It is synthesized from cysteine by cystathionine γ-lyase (CGL) and cystathionine β-synthase (CBS). The present study examined the benefits of exogenous H2S on renal ischemia reperfusion (IR) injury, as well as the effects of CGL or CBS inhibition. Furthermore, we elucidated the mechanism underlying the action of H2S in the kidneys. MATERIALS AND METHODS: Thirty male Sprague-Dawley rats were randomly assigned to five groups: a sham, renal IR control, sodium hydrosulfide (NaHS) treatment, H2S donor, and CGL or CBS inhibitor administration group. Levels of blood urea nitrogen (BUN), serum creatinine (Cr), renal tissue malondialdehyde (MDA), and superoxide dismutase (SOD) were estimated. Histological changes, apoptosis, and expression of mitogen-activated protein kinase (MAPK) family members (extracellular signal-regulated kinase, c-Jun N-terminal kinase, and p38) were also evaluated. RESULTS: NaHS attenuated serum BUN and Cr levels, as well as histological damage caused by renal IR injury. Administration of NaHS also reduced oxidative stress as evident from decreased MDA, preserved SOD, and reduced apoptotic cells. Additionally, NaHS prevented renal IR-induced MAPK phosphorylation. The CGL or CBS group showed increased MAPK family activity; however, there was no significant difference in the IR control group. CONCLUSION: Exogenous H2S can mitigate IR injury-led renal damage. The proposed beneficial effect of H2S is, in part, because of the anti-oxidative stress associated with modulation of the MAPK signaling pathways.
