Neuroprotective Effect of Astragalus Polysacharin on Streptozotocin (STZ)-Induced Diabetic Rats.
Animals
Astragalus Plant
/ chemistry
Calcium-Calmodulin-Dependent Protein Kinase Type 2
/ analysis
Cognitive Dysfunction
/ metabolism
Cyclic AMP Response Element-Binding Protein
/ analysis
Diabetes Mellitus, Experimental
/ metabolism
Drugs, Chinese Herbal
/ pharmacology
Hippocampus
/ metabolism
Male
Maze Learning
/ drug effects
Memory
/ drug effects
Neuroprotective Agents
/ pharmacology
Plant Extracts
/ pharmacology
Plant Roots
/ chemistry
Rats
Rats, Sprague-Dawley
Receptors, N-Methyl-D-Aspartate
/ analysis
Streptozocin
Journal
Medical science monitor : international medical journal of experimental and clinical research
ISSN: 1643-3750
Titre abrégé: Med Sci Monit
Pays: United States
ID NLM: 9609063
Informations de publication
Date de publication:
05 Jan 2019
05 Jan 2019
Historique:
entrez:
6
1
2019
pubmed:
6
1
2019
medline:
21
3
2019
Statut:
epublish
Résumé
BACKGROUND In the recent years, there has been increasing interest in traditional Chinese medicine as a neuroprotective nutrient in the management of chronic neurodegenerative disease, such as diabetic cognitive decline. Astragalus polysacharin (APS), a Chinese herb extract, is a biologically active treatment for neurodegenerative diseases. Therefore, in the present study, we investigated the neuroprotective effects of APS (20 mg/kg) on diabetes-induced memory impairments in Sprague-Dawley (SD) rats and explored its underlying mechanisms of action. MATERIAL AND METHODS Thirty SD rats were randomly divided into a control group (CON group, n=10), a diabetic model (DM) group (n=10), and an APS group (n=10). We administered 55 mg/kg streptozotocin (STZ, Sigma) by intraperitoneal injection to induce a diabetic model. Food and water intake, body weight, and blood fasting plasma glucose (FPG) were measured. The Morris water maze test (MWM) was used to assess learning and memory ability, and we measured levels of N-methyl-D-aspartate receptor (NMDA), calcium/calmodulin-dependent protein kinase II (CaMKII), and cAMP response element-binding protein (CREB) in the hippocampus. RESULTS APS (20 mg/kg) administration decreased the rats' fasting plasma glucose (FPG) levels and body weight. APS (20 mg/kg) administration improved the cognitive performance of diabetes-induced rats in the Morris water maze test. APS (20 mg/kg) administration reduced the number of dead cells in the CA1 region of the hippocampus. Furthermore, APS (20 mg/kg) administration obviously upregulated the phosphorylation levels CREB, NMDA, and CaMK II. CONCLUSIONS These results suggest that APS has the neuroprotective effects, and it may be a candidate for treatment of neurodegenerative diseases such as diabetic cognitive impairment.
Identifiants
pubmed: 30610831
pii: 912213
doi: 10.12659/MSM.912213
pmc: PMC6330021
doi:
Substances chimiques
Creb1 protein, rat
0
Cyclic AMP Response Element-Binding Protein
0
Drugs, Chinese Herbal
0
Neuroprotective Agents
0
Plant Extracts
0
Receptors, N-Methyl-D-Aspartate
0
Streptozocin
5W494URQ81
Calcium-Calmodulin-Dependent Protein Kinase Type 2
EC 2.7.11.17
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
135-141Références
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