Evaluating the protective role of trimetazidine versus nano-trimetazidine in amelioration of bilateral renal ischemia/reperfusion induced neuro-degeneration: Implications of ERK1/2, JNK and Galectin-3 /NF-κB/TNF-α/HMGB-1 signaling.
Brain
Galectin-3, HMGB-1
Nano-Trimetazidine
Oxidative stress
Journal
Tissue & cell
ISSN: 1532-3072
Titre abrégé: Tissue Cell
Pays: Scotland
ID NLM: 0214745
Informations de publication
Date de publication:
Dec 2023
Dec 2023
Historique:
received:
07
08
2023
revised:
24
09
2023
accepted:
13
10
2023
medline:
13
11
2023
pubmed:
22
10
2023
entrez:
21
10
2023
Statut:
ppublish
Résumé
Renal ischemia/reperfusion (I/R) is a primary culprit of acute kidney injury. Neurodegeneration can result from I/R, but the mechanisms are still challenging. We studied the implications of bilateral renal I/R on brain and potential involvement of the oxidative stress (OS) driven extracellular signal-regulated kinase1/2, c-Jun N-terminal kinase (ERK1/2, JNK) and Galectin-3 (Gal-3)/nuclear factor Kappa B (NF-қB)/tumor necrosis factor-alpha (TNF-α), high mobility group box-1 (HMGB-1), and caspase-3 paths upregulation. We tested the impact of Nano-trimetazidine (Nano-TMZ) on these pathways being a target of its neuroprotective effects. Study groups; Sham, I/R, TMZ+I/R, and Nano-TMZ+I/R. Kidney functions, cognition, hippocampal OS markers, Gal-3, NF-қB, p65 and HMGB-1 gene expression, TNF-α level, t-JNK/p-JNK and t-ERK/p-ERK proteins, caspase-3, glial fibrillary acidic protein (GFAP) and ionized calcium binding protein-1 (Iba-1) were assessed. Nano-TMZ averted renal I/R-induced hippocampal impairment by virtue of its anti: oxidative, inflammatory, and apoptotic properties. Nano-TMZ is more than anti-ischemic.
Sections du résumé
BACKGROUND
BACKGROUND
Renal ischemia/reperfusion (I/R) is a primary culprit of acute kidney injury. Neurodegeneration can result from I/R, but the mechanisms are still challenging. We studied the implications of bilateral renal I/R on brain and potential involvement of the oxidative stress (OS) driven extracellular signal-regulated kinase1/2, c-Jun N-terminal kinase (ERK1/2, JNK) and Galectin-3 (Gal-3)/nuclear factor Kappa B (NF-қB)/tumor necrosis factor-alpha (TNF-α), high mobility group box-1 (HMGB-1), and caspase-3 paths upregulation. We tested the impact of Nano-trimetazidine (Nano-TMZ) on these pathways being a target of its neuroprotective effects.
METHODS
METHODS
Study groups; Sham, I/R, TMZ+I/R, and Nano-TMZ+I/R. Kidney functions, cognition, hippocampal OS markers, Gal-3, NF-қB, p65 and HMGB-1 gene expression, TNF-α level, t-JNK/p-JNK and t-ERK/p-ERK proteins, caspase-3, glial fibrillary acidic protein (GFAP) and ionized calcium binding protein-1 (Iba-1) were assessed.
RESULTS
RESULTS
Nano-TMZ averted renal I/R-induced hippocampal impairment by virtue of its anti: oxidative, inflammatory, and apoptotic properties.
CONCLUSION
CONCLUSIONS
Nano-TMZ is more than anti-ischemic.
Identifiants
pubmed: 37865040
pii: S0040-8166(23)00229-X
doi: 10.1016/j.tice.2023.102241
pii:
doi:
Substances chimiques
Trimetazidine
N9A0A0R9S8
NF-kappa B
0
Tumor Necrosis Factor-alpha
0
Galectin 3
0
Caspase 3
EC 3.4.22.-
HMGB Proteins
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
102241Informations de copyright
Copyright © 2023 Elsevier Ltd. All rights reserved.