Mitochondrial Protection and Against Glutamate Neurotoxicity via Shh/Ptch1 Signaling Pathway to Ameliorate Cognitive Dysfunction by Kaixin San in Multi-Infarct Dementia Rats.
Animals
Cognitive Dysfunction
/ chemically induced
Dementia, Multi-Infarct
/ chemically induced
Disease Models, Animal
Drugs, Chinese Herbal
/ pharmacology
Glutamic Acid
/ metabolism
Male
Memory Disorders
/ chemically induced
Mitochondria
/ drug effects
Neurons
/ drug effects
Patched-1 Receptor
/ drug effects
Rats, Sprague-Dawley
Signal Transduction
/ drug effects
Journal
Oxidative medicine and cellular longevity
ISSN: 1942-0994
Titre abrégé: Oxid Med Cell Longev
Pays: United States
ID NLM: 101479826
Informations de publication
Date de publication:
2021
2021
Historique:
received:
19
02
2021
accepted:
17
06
2021
entrez:
26
7
2021
pubmed:
27
7
2021
medline:
31
12
2021
Statut:
epublish
Résumé
Multi-infarct dementia (MID), a prominent subtype of vascular dementia (VD), is responsible for at least 15 to 20 percent of dementia in the elderly. Mitochondrial dysfunctions and glutamate neurotoxicity due to chronic hypoperfusion and oxidative stress were regarded as the major risk factors in the pathogenesis.
Identifiants
pubmed: 34306310
doi: 10.1155/2021/5590745
pmc: PMC8285175
doi:
Substances chimiques
Drugs, Chinese Herbal
0
Patched-1 Receptor
0
Ptch1 protein, rat
0
kaixin
0
Glutamic Acid
3KX376GY7L
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
5590745Informations de copyright
Copyright © 2021 Xiaoqiong Li et al.
Déclaration de conflit d'intérêts
The authors declare that there is no conflict of interest regarding the publication of this paper.
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