Hydrogen sulfide accelerates the recovery of kidney tubules after renal ischemia/reperfusion injury.
- Alternative Author(s)
- Kim, Jee In
- Publication Year
- CBS; CSE; Hydrogen sulfide; Ischemia; Reactive oxygen species; Regeneration
- Background. Progression of acute kidney injury to chronic
kidney disease (CKD) is associated with inadequate recovery
of damaged kidney. Hydrogen sulfide (H2S) regulates a variety
of cellular signals involved in cell death, differentiation and
proliferation. This study aimed to identify the role of H2S and
its producing enzymes in the recovery of kidney following ischemia/
reperfusion (I/R) injury.
Methods. Mice were subjected to 30 min of bilateral renal ischemia.
Some mice were administered daily NaHS, an H2S
donor, and propargylglycine (PAG), an inhibitor of the H2Sproducing
enzyme cystathionine gamma-lyase (CSE), during
the recovery phase. Cell proliferation was assessed via 50-bromo-
20-deoxyuridine (BrdU) incorporation assay.
Results. Ischemia resulted in decreases in CSE and cystathionine
beta-synthase (CBS) expression and activity, and H2S
level in the kidney. These decreases did not return to sham
level until 8 days after ischemia when kidney had fibrotic lesions.
NaHS administration to I/R-injured mice accelerated
the recovery of renal function and tubule morphology, whereas
PAG delayed that. Furthermore, PAG increased mortality after
ischemia. NaHS administration to I/R-injured mice accelerated
tubular cell proliferation, whereas it inhibited interstitial cell
proliferation. In addition, NaHS treatment reduced post-I/R
superoxide formation, lipid peroxidation, level of GSSG/GSH
and Nox4 expression, whereas it increased catalase and MnSOD
Conclusions. Our findings demonstrate that H2S accelerates
the recovery of I/R-induced kidney damage, suggesting that
the H2S-producing transsulfuration pathway plays an important
role in kidney repair after acute injury.
Keywords: CBS, CSE, hydrogen sulfide, ischemia, reactive
oxygen species, regeneration
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