title: Protective Effects of Hydrogen Sulfide in the Ageing Kidney.
abstract: Aims. The study aimed to examine whether hydrogen sulfide (H2S) generation changed in the kidney of the ageing mouse and its relationship with impaired kidney function.Results. H2S levels in the plasma, urine, and kidney decreased significantly in ageing mice. The expression of two known H2S-producing enzymes in kidney, cystathionineγ-lyase (CSE) and cystathionine-β-synthase (CBS), decreased significantly during ageing. Chronic H2S donor (NaHS, 50μmol/kg/day, 10 weeks) treatment could alleviate oxidative stress levels and renal tubular interstitial collagen deposition. These protective effects may relate to transcription factor Nrf2 activation and antioxidant proteins such as HO-1, SIRT1, SOD1, and SOD2 expression upregulation in the ageing kidney after NaHS treatment. Furthermore, the expression of H2S-producing enzymes changed with exogenous H2S administration and contributed to elevated H2S levels in the ageing kidney.Conclusions. Endogenous hydrogen sulfide production in the ageing kidney is insufficient. Exogenous H2S can partially rescue ageing-related kidney dysfunction by reducing oxidative stress, decreasing collagen deposition, and enhancing Nrf2 nuclear translocation. Recovery of endogenous hydrogen sulfide production may also contribute to the beneficial effects of NaHS treatment.
authors.affiliation: Research Center on Aging and Medicine, Fudan University, Shanghai Key Laboratory of Bioactive Small Molecules, Department of Physiology and Pathophysiology, Shanghai Medical College, Fudan University, Shanghai, China.
authors.forename: Cui-Lan
authors.initials: CL
authors.lastname: Hou
authors.affiliation: Research Center on Aging and Medicine, Fudan University, Shanghai Key Laboratory of Bioactive Small Molecules, Department of Physiology and Pathophysiology, Shanghai Medical College, Fudan University, Shanghai, China.
authors.forename: Ming-Jie
authors.initials: MJ
authors.lastname: Wang
authors.affiliation: Research Center on Aging and Medicine, Fudan University, Shanghai Key Laboratory of Bioactive Small Molecules, Department of Physiology and Pathophysiology, Shanghai Medical College, Fudan University, Shanghai, China.
authors.forename: Chen
authors.initials: C
authors.lastname: Sun
authors.affiliation: Research Center on Aging and Medicine, Fudan University, Shanghai Key Laboratory of Bioactive Small Molecules, Department of Physiology and Pathophysiology, Shanghai Medical College, Fudan University, Shanghai, China.
authors.forename: Yong
authors.initials: Y
authors.lastname: Huang
authors.affiliation: Research Center on Aging and Medicine, Fudan University, Shanghai Key Laboratory of Bioactive Small Molecules, Department of Physiology and Pathophysiology, Shanghai Medical College, Fudan University, Shanghai, China.
authors.forename: Sheng
authors.initials: S
authors.lastname: Jin
authors.affiliation: Research Center on Aging and Medicine, Fudan University, Shanghai Key Laboratory of Bioactive Small Molecules, Department of Physiology and Pathophysiology, Shanghai Medical College, Fudan University, Shanghai, China.
authors.forename: Xue-Pan
authors.initials: XP
authors.lastname: Mu
authors.affiliation: Research Center on Aging and Medicine, Fudan University, Shanghai Key Laboratory of Bioactive Small Molecules, Department of Physiology and Pathophysiology, Shanghai Medical College, Fudan University, Shanghai, China.
authors.forename: Ying
authors.initials: Y
authors.lastname: Chen
authors.affiliation: Research Center on Aging and Medicine, Fudan University, Shanghai Key Laboratory of Bioactive Small Molecules, Department of Physiology and Pathophysiology, Shanghai Medical College, Fudan University, Shanghai, China.
authors.forename: Yi-Chun
authors.identifier: 0000-0002-0873-2957
authors.initials: YC
authors.lastname: Zhu
mesh_terms: D021581:Active Transport, Cell Nucleus; D000367:Age Factors; D000375:Aging / Q000097:blood / Q000378:metabolism* / Q000473:pathology / Q000652:urine; D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D003094:Collagen / Q000378:metabolism; D003541:Cystathionine beta-Synthase / Q000378:metabolism; D003542:Cystathionine gamma-Lyase / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D004789:Enzyme Activation; D005355:Fibrosis; D051547:Heme Oxygenase-1 / Q000378:metabolism; D006862:Hydrogen Sulfide / Q000097:blood / Q000378:metabolism* / Q000652:urine; D007668:Kidney / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D008297:Male; D008565:Membrane Proteins / Q000378:metabolism; D008810:Mice, Inbred C57BL; D051267:NF-E2-Related Factor 2 / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects; D015398:Signal Transduction / Q000187:drug effects; D056564:Sirtuin 1 / Q000378:metabolism; D013440:Sulfides / Q000378:metabolism / Q000494:pharmacology*; D013482:Superoxide Dismutase / Q000378:metabolism; D000072105:Superoxide Dismutase-1 / Q000378:metabolism; D000099156:Superoxide Dismutase 2
chemical_list: D003094:Collagen; D003541:Cystathionine beta-Synthase; D003542:Cystathionine gamma-Lyase; D051547:Heme Oxygenase-1; D006862:Hydrogen Sulfide; D008565:Membrane Proteins; D051267:NF-E2-Related Factor 2; D056564:Sirtuin 1; D013440:Sulfides; D013482:Superoxide Dismutase; D000072105:Superoxide Dismutase-1; D000099156:Superoxide Dismutase 2; C495636:Nfe2l2 protein, mouse; C496542:Hmox1 protein, mouse; C000606291:Sod1 protein, mouse; C470545:Sirt1 protein, mouse; C025451:sodium bisulfide