Oral Administration of Lipopolysaccharide Prevents Cognitive Impairment in Streptozotocin-induced Diabetic Mice in a Blood Glucose-independent Manner.
Administration, Oral
Animals
Blood Glucose
/ drug effects
Chemokine CCL7
/ genetics
Cognitive Dysfunction
/ blood
Diabetes Mellitus, Experimental
/ blood
Diabetes Mellitus, Type 1
/ blood
HSP40 Heat-Shock Proteins
/ genetics
Lipopolysaccharides
/ pharmacology
Male
Mice, Inbred C57BL
Microglia
/ drug effects
Neuroprotective Agents
/ pharmacology
Lipopolysaccharide (LPS)
cognitive impairment
dementia
diabetes
microglia
oral administration
streptozotocin (STZ)
Journal
Anticancer research
ISSN: 1791-7530
Titre abrégé: Anticancer Res
Pays: Greece
ID NLM: 8102988
Informations de publication
Date de publication:
Aug 2021
Aug 2021
Historique:
received:
21
05
2021
revised:
03
06
2021
accepted:
04
06
2021
entrez:
20
7
2021
pubmed:
21
7
2021
medline:
30
7
2021
Statut:
ppublish
Résumé
Diabetes is a risk factor for dementia. However, no radical preventive method for diabetes-associated dementia has yet been developed. Our previous study revealed that oral administration of lipopolysaccharide (LPS) prevents high-fat diet-induced cognitive impairment. Therefore, we investigated here whether oral administration of LPS (OAL) could also prevent diabetes-associated dementia. Diabetic mice were produced by intraperitoneal administration of streptozotocin (STZ), and then mice were orally administered LPS. Cognitive ability was evaluated using the Morris water maze, and gene expression was analyzed in isolated microglia. OAL prevented STZ-induced diabetic cognitive impairment, but did not affect blood glucose levels. Moreover, OAL promoted the expression of neuroprotective genes in microglia, such as heat shock protein family 40 (HSP40) and chemokine CCL7. OAL prevents diabetes-associated dementia, potentially via promotion of HSP40 and CCL7 expression in microglia.
Sections du résumé
BACKGROUND/AIM
OBJECTIVE
Diabetes is a risk factor for dementia. However, no radical preventive method for diabetes-associated dementia has yet been developed. Our previous study revealed that oral administration of lipopolysaccharide (LPS) prevents high-fat diet-induced cognitive impairment. Therefore, we investigated here whether oral administration of LPS (OAL) could also prevent diabetes-associated dementia.
MATERIALS AND METHODS
METHODS
Diabetic mice were produced by intraperitoneal administration of streptozotocin (STZ), and then mice were orally administered LPS. Cognitive ability was evaluated using the Morris water maze, and gene expression was analyzed in isolated microglia.
RESULTS
RESULTS
OAL prevented STZ-induced diabetic cognitive impairment, but did not affect blood glucose levels. Moreover, OAL promoted the expression of neuroprotective genes in microglia, such as heat shock protein family 40 (HSP40) and chemokine CCL7.
CONCLUSION
CONCLUSIONS
OAL prevents diabetes-associated dementia, potentially via promotion of HSP40 and CCL7 expression in microglia.
Identifiants
pubmed: 34281874
pii: 41/8/4053
doi: 10.21873/anticanres.15206
doi:
Substances chimiques
Blood Glucose
0
Ccl7 protein, mouse
0
Chemokine CCL7
0
Dnajb1 protein, mouse
0
HSP40 Heat-Shock Proteins
0
Lipopolysaccharides
0
Neuroprotective Agents
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
4053-4059Informations de copyright
Copyright © 2021 International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.