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Ameliorative Effects of Hydrogen Sulfide (Nahs) on Chronic Kidney Disease-Induced Brain Dysfunction in Rats: Implication on Role of Nitric Oxide (No) Signaling Publisher Pubmed



Askari H1 ; Abazari MF2 ; Ghoraeian P2 ; Torabinejad S2 ; Nouri Aleagha M2 ; Mirfallah Nassiri R3 ; Tahmasebi F3 ; Abedi N4 ; Rajani SF5 ; Salarian A1 ; Belaran M6 ; Elshiekh M7 ; Sanadgol N8
Authors
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Authors Affiliations
  1. 1. Department of Physiology, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran
  2. 2. Department of Genetics, Tehran Medical Sciences Branch, Islamic Azad University, Tehran, Iran
  3. 3. Faculty of Sports Science, Shahid Rajaee Teacher Training University, Tehran, Iran
  4. 4. College of Veterinary Medicine, Western University of Health Sciences, Pomona, CA, United States
  5. 5. Department of Physiology, School of Medicine, International Campus, Tehran University of Medical Sciences, Tehran, Iran
  6. 6. Department of Physiology, Faculty of Medicine, Zabol University of Medical Sciences, Zabol, Iran
  7. 7. Department of Physiology, Faculty of Medicine, University of Dongola, Dongola, Sudan
  8. 8. Department of Biology, Faculty of Sciences, University of Zabol, Zabol, Iran

Source: Metabolic Brain Disease Published:2018


Abstract

Chronic kidney disease (CKD) is a major public health problem worldwide and is associated with spatial learning deficits. The aim of the present study was to evaluate the protective effects of hydrogen sulfide (H2S) on CKD-mediated behavioral deficits with emphasis to the role of nitric oxide (NO) in these effects. Fifty rats were randomly allocated to five experimental groups including: sham, Five-sixth (5/6) nephrectomy (Nx), 5/6Nx + NaHS, 5/6Nx + NaHS+L-nitroarginine methyl ester (L-NAME), and 5/6Nx + NaHS+aminoguanidine (AMG). Twelve weeks after 5/6Nx, we evaluated proteinuria, creatinine clearance (CrCl), oxidative/antioxidant status, and hippocampus neuro-inflammation and NO synthase genes in all groups. Furthermore, training trials of all animals were conducted in the Morris water maze (MWM) task one day before animal euthanizing. As predicted, 5/6Nx induced several injuries, including enhancement of proteinuria and reduction of CCr, oxidant/antioxidant imbalance and up-regulation of TNF-α and IL-1β gene expressions in the hippocampus tissues. As predicted, 5/6Nx resulted in learning and memory impairments, and increased escape latency during acquisition trials in the MWM task. Interestingly, NaHS (H2S donor) improved behavioral deficits, renal dysfunction, accelerated anti-oxidant/anti-inflammatory responses and increased eNOS and decreased iNOS. Moreover, these effects of NaHS were prevented by L-NAME but not AMG co-administration. In conclusion, H2S ameliorates CKD-mediated brain dysfunctions, through interaction with NO signaling in the hippocampus. © 2018, Springer Science+Business Media, LLC, part of Springer Nature.
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