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  • Hydrogen sulfide accelerates the recovery of kidney tubules after renal ischemia/reperfusion injury.

Hydrogen sulfide accelerates the recovery of kidney tubules after renal ischemia/reperfusion injury.

Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association (2015-07-05)
Sang Jun Han, Jee In Kim, Jeen-Woo Park, Kwon Moo Park
摘要

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. 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 H2S-producing enzyme cystathionine gamma-lyase (CSE), during the recovery phase. Cell proliferation was assessed via 5'-bromo-2'-deoxyuridine (BrdU) incorporation assay. 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 expression. 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.

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Sigma-Aldrich
2-硫代巴比妥酸, ≥98%
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L -赖氨酸, ≥98% (TLC)
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肌酸酐, anhydrous, ≥98%
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吡哆醛5'-磷酸盐 水合物, ≥98%
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氢硫酸, ≥99.5%
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锰, powder, ≥99.9% trace metals basis
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吡哆醛5'-磷酸盐 一水合物, ≥97.0% (NT)
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二氢乙锭, ≥95%
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L -赖氨酸, crystallized, ≥98.0% (NT)
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吡哆醛5'-磷酸盐 水合物, powder, BioReagent, suitable for cell culture
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二氢乙锭, BioReagent, suitable for fluorescence, ≥95% (HPCE)
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DL-炔丙基甘氨酸, cystathionine γ-lyase inhibitor
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锰, powder, −325 mesh, ≥99% trace metals basis
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DL-胱硫醚, ≥90% (HPLC)
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锰, chips, thickness <2.0 mm, 99%
锰, rod, 10mm, diameter 4.0mm, cast, 99.5%
锰, foil, 25x25mm, thickness 2mm, hot-pressed, 99.95%
锰, foil, 50x50mm, thickness 2mm, hot-pressed, 99.95%
锰, foil, not light tested, 100x100mm, thickness 0.0125mm, permanent polyester support, 98.7%
锰, foil, not light tested, 100x100mm, thickness 0.01mm, permanent polyester support, 98.7%
锰, foil, not light tested, 100x100mm, thickness 0.025mm, permanent polyester support, 98.7%
锰, foil, not light tested, 100x100mm, thickness 0.02mm, permanent polyester support, 98.7%
锰, foil, not light tested, 25x25mm, thickness 0.001mm, permanent polyester support, 98.7%
锰, foil, not light tested, 25x25mm, thickness 0.0025mm, permanent polyester support, 98.7%
锰, foil, not light tested, 25x25mm, thickness 0.002mm, permanent polyester support, 98.7%
锰, foil, not light tested, 25x25mm, thickness 0.003mm, permanent polyester support, 98.7%
锰, foil, not light tested, 25x25mm, thickness 0.004mm, permanent polyester support, 98.7%
锰, foil, not light tested, 25x25mm, thickness 0.005mm, permanent polyester support, 98.7%
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锰, foil, not light tested, 25x25mm, thickness 0.007mm, permanent polyester support, 98.7%