RIPK1 inhibitor Cpd-71 attenuates renal dysfunction in cisplatin-treated mice via attenuating necroptosis, inflammation and oxidative stress.
Acute Kidney Injury
/ drug therapy
Animals
Antineoplastic Agents
/ administration & dosage
Cisplatin
/ adverse effects
Humans
Kidney
/ drug effects
Male
Mice
Mice, Inbred C57BL
Necroptosis
/ drug effects
Oxidative Stress
/ drug effects
Protein Kinase Inhibitors
/ administration & dosage
Receptor-Interacting Protein Serine-Threonine Kinases
/ antagonists & inhibitors
RIPK1 inhibitor
actue kidney injury
inflammation
necroptosis
oxidative stress
Journal
Clinical science (London, England : 1979)
ISSN: 1470-8736
Titre abrégé: Clin Sci (Lond)
Pays: England
ID NLM: 7905731
Informations de publication
Date de publication:
31 07 2019
31 07 2019
Historique:
received:
08
06
2019
revised:
12
07
2019
accepted:
17
07
2019
pubmed:
19
7
2019
medline:
9
4
2020
entrez:
19
7
2019
Statut:
epublish
Résumé
Acute kidney injury (AKI) is a destructive clinical condition induced by multiple insults including ischemic reperfusion, nephrotoxic drugs and sepsis. It is characterized by a sudden decline in renal function, in addition to excessive inflammation, oxidative stress and programmed cell death of renal tubular epithelial cells. RIPK1-mediated necroptosis plays an important role in AKI. In the present study, we evaluated the treatment effects of Compound-71 (Cpd-71), a novel RIPK1 inhibitor, by comparing with Necrostatin-1 (Nec-1), a classic RIPK1 inhibitor, which has several drawbacks like the narrow structure-activity relationship (SAR) profile, moderate potency and non-ideal pharmacokinetic properties,
Identifiants
pubmed: 31315969
pii: CS20190599
doi: 10.1042/CS20190599
doi:
Substances chimiques
Antineoplastic Agents
0
Protein Kinase Inhibitors
0
Receptor-Interacting Protein Serine-Threonine Kinases
EC 2.7.11.1
Ripk1 protein, mouse
EC 2.7.11.1
Cisplatin
Q20Q21Q62J
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1609-1627Informations de copyright
© 2019 The Author(s). Published by Portland Press Limited on behalf of the Biochemical Society.