Phoenixin 14 ameloriates pancreatic injury in streptozotocin-induced diabetic rats by alleviating oxidative burden.
MPO
free radicals
gastric emptying
glucose
inflammation
insulin
Journal
The Journal of pharmacy and pharmacology
ISSN: 2042-7158
Titre abrégé: J Pharm Pharmacol
Pays: England
ID NLM: 0376363
Informations de publication
Date de publication:
04 Nov 2022
04 Nov 2022
Historique:
received:
17
03
2022
accepted:
04
07
2022
pubmed:
22
9
2022
medline:
9
11
2022
entrez:
21
9
2022
Statut:
ppublish
Résumé
Phoenixin-14 (PNX) is a neuropeptide that has been shown to prevent oxidative damage and stimulates insulin secretion. We investigated the effects of PNX on pancreatic injury induced by streptozotocin (STZ), and nicotinamide (NAD). Male Sprague-Dawley rats, in control (C) and diabetic (STZ) groups, were treated with either saline, or PNX (0.45 nmol/kg, or 45 nmol/kg) daily for 3 days 1 week after STZ injection. Fasting blood glucose (FBG) and gastric emptying rate (GER) were measured. Tissue and blood samples were collected. PNX treatments prevented pancreatic damage and β cell loss. Increased luminol and lucigenin levels in the pancreas, ileum and liver tissues of STZ groups were alleviated by PNX treatment in pancreatic and ileal tissues. PNX0.45 decreased FBG without any change in insulin blood level and pancreatic mRNA. GER increased in all diabetic rats while PNX0.45 delayed GER only in the C group. PNX diminishes pancreatic damage and lowers FBG by reducing oxidative load.
Identifiants
pubmed: 36130115
pii: 6706884
doi: 10.1093/jpp/rgac055
doi:
Substances chimiques
Streptozocin
5W494URQ81
Insulin
0
Blood Glucose
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
1651-1659Subventions
Organisme : The Scientific and Technological Research Council of Türkiye
Organisme : Foundation of Marmara University School of Medicine
Organisme : Abdi Ibrahim Pharmaceutical Ltd
Informations de copyright
© The Author(s) 2022. Published by Oxford University Press on behalf of the Royal Pharmaceutical Society. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.