Phycocyanin alleviates ICV-STZ induced cognitive and molecular deficits via PI3-Kinase dependent pathway.
Alzheimer Disease
/ drug therapy
Animals
Brain
/ drug effects
Brain-Derived Neurotrophic Factor
/ genetics
Choline O-Acetyltransferase
/ genetics
Cognition
/ drug effects
Disease Models, Animal
Hippocampus
/ drug effects
Humans
Infusions, Intraventricular
Insulin Receptor Substrate Proteins
/ genetics
Male
Neuroprotective Agents
/ administration & dosage
Phosphatidylinositol 3-Kinases
/ genetics
Phycocyanin
/ administration & dosage
Rats
Rats, Wistar
Signal Transduction
/ drug effects
Streptozocin
/ administration & dosage
Alzheimer's disease
Insulin signaling
Neuroprotective
Spirulina
Journal
Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association
ISSN: 1873-6351
Titre abrégé: Food Chem Toxicol
Pays: England
ID NLM: 8207483
Informations de publication
Date de publication:
Nov 2020
Nov 2020
Historique:
received:
31
05
2020
revised:
29
07
2020
accepted:
10
08
2020
pubmed:
18
8
2020
medline:
14
5
2021
entrez:
18
8
2020
Statut:
ppublish
Résumé
In this study, the effect of Phycocyanin (Pc) to ameliorate the cognitive dysfunction in experimental model of Alzheimer's disease (AD) was evaluated. Intracerebroventricular (ICV) induction of Streptozotocin (STZ) (3 mg/kg) was done bilaterally twice in rats on alternative days. Rats were injected with Pc (50, 100 mg/kg; i. p.) for 28 days daily for behavioural and cholinergic activity assessment. As the effect was only significant at 100 mg/kg, later molecular experiments were performed using the same only. STZ induction led to increased activity of hippocampal cholinesterases and BAX and decreased activity of BCL-2 and ChAT. It enhanced TNF-α, and NF-κB in rat's brain and reduced BDNF and IGF-1 levels. Dysfunctional insulin signaling and decreased gene expressions of PI3-K, AKT was also observed. However, Pc treatment significantly prevented STZ-induced increased activity of hippocampal cholinesterases and BAX as well as increased the levels of BCL-2 and ChAT. Neuroinflammation was significantly attenuated and BDNF and IGF-1 levels were upregulated. Further, Pc also alleviated dysfunctional insulin signaling as evidenced by increased gene expression of IRS-1, PI3-K, AKT. In conclusion, our study demonstrated the immense potential of Pc in attenuating STZ-induced cognitive decline and it may be further explored as a therapeutic agent in managing AD.
Identifiants
pubmed: 32805344
pii: S0278-6915(20)30574-3
doi: 10.1016/j.fct.2020.111684
pii:
doi:
Substances chimiques
Brain-Derived Neurotrophic Factor
0
Insulin Receptor Substrate Proteins
0
Neuroprotective Agents
0
Phycocyanin
11016-15-2
Streptozocin
5W494URQ81
Choline O-Acetyltransferase
EC 2.3.1.6
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
111684Informations de copyright
Copyright © 2020 Elsevier Ltd. All rights reserved.