In:
Oxidative Medicine and Cellular Longevity, Hindawi Limited, Vol. 2016 ( 2016), p. 1-15
Abstract:
Background . The study was designed to investigate if H 2 S could inhibit high-salt diet-induced renal excessive oxidative stress and kidney injury in Dahl rats. Methods . Male salt-sensitive Dahl and SD rats were used. Blood pressure (BP), serum creatinine, urea, creatinine clearance rate, and 24-hour urine protein were measured. Renal ultra- and microstructures were observed. Collagen-I and -III contents the oxidants and antioxidants levels in renal tissue were detected. Keap1/Nrf2 association and Keap1 s-sulfhydration were detected. Results . After 8 weeks of high-salt diet, BP was significantly increased, renal function and structure were impaired, and collagen deposition was abundant in renal tissues with increased renal MPO activity, H 2 O 2 , MDA, GSSG, and • OH contents, reduced renal T-AOC and GSH contents, CAT, GSH-PX and SOD activity, and SOD expressions in Dahl rats. Furthermore, endogenous H 2 S in renal tissues was decreased in Dahl rats. H 2 S donor, however, decreased BP, improved renal function and structure, and inhibited collagen excessive deposition in kidney, in association with increased antioxidative activity and reduced oxidative stress in renal tissues. H 2 S activated Nrf2 by inducing Keap1 s-sulfhydration and subsequent Keap1/Nrf2 disassociation. Conclusions . H 2 S protected against high-salt diet-induced renal injury associated with enhanced antioxidant capacity and inhibited renal oxidative stress.
Type of Medium:
Online Resource
ISSN:
1942-0900
,
1942-0994
DOI:
10.1155/2016/2807490
Language:
English
Publisher:
Hindawi Limited
Publication Date:
2016
detail.hit.zdb_id:
2455981-7
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