Telmisartan Treatment Ameliorates Memory Deficits in Streptozotocin-Induced Diabetic Mice via Attenuating Cerebral Amyloidosis

Autor: Chao Wang, Ming Xing Miao, Hao Hong, Guang Jun Liu, Zhen Lin Mei, Yan Long, Guan Tao Du, Meng Hu, Jia Chang Li, Mei Hu
Jazyk: angličtina
Rok vydání: 2014
Předmět:
Male
medicine.medical_specialty
endocrine system diseases
Receptor for Advanced Glycation End Products
Central nervous system
Administration
Oral
Hippocampus
Morris water navigation task
Benzoates
Streptozocin
Diabetes Mellitus
Experimental
Amyloid beta-Protein Precursor
Mice
Oral administration
Internal medicine
Animals
Aspartic Acid Endopeptidases
Medicine
Telmisartan
Cerebral Cortex
Pharmacology
Memory Disorders
Mice
Inbred ICR
Type 1 diabetes
Amyloid beta-Peptides
business.industry
lcsh:RM1-950
Transcription Factor RelA
nutritional and metabolic diseases
Streptozotocin
medicine.disease
Angiotensin II
Peptide Fragments
Cerebral Amyloid Angiopathy
Disease Models
Animal
Diabetes Mellitus
Type 1
Treatment Outcome
Endocrinology
medicine.anatomical_structure
lcsh:Therapeutics. Pharmacology
Molecular Medicine
Benzimidazoles
Amyloid Precursor Protein Secretases
business
Angiotensin II Type 1 Receptor Blockers
medicine.drug
Zdroj: Journal of Pharmacological Sciences, Vol 124, Iss 4, Pp 418-426 (2014)
ISSN: 1347-8613
Popis: Telmisartan, an angiotensin II type 1–receptor blocker (ARBs), has been reported to exert beneficial effects on the central nervous system (CNS). However, the effect of telmisartan on cognitive impairment associated with type 1 diabetes is not well known. Here, we examined the possibility that telmisartan could improve memory function in a type 1 diabetic mouse model, streptozotocin (STZ)-induced diabetic mice. STZ-induced diabetic mice subjected to the Morris Water Maze (MWM) task exhibited a significant decline of spatial learning and memory. Oral administration of telmisartan at two nonhypotensive doses (0.7 or 0.35 mg/kg) significantly improved memory deficits in STZ-induced diabetic mice. Telmisartan treatment markedly reduced Aβ42, APP, BACE1, RAGE, and NF-κB p65 of the hippocampus and cortex, but did not beneficially affect hyperglycemia and hypoinsulinemia in the STZ-induced diabetic mice compared with untreated diabetic mice. Taken together, our findings suggest that telmisartan ameliorates memory deficits in type 1 diabetic mice, at least partly because of attenuation of amyloidosis in the brain. Keywords:: type 1 diabetes, telmisartan, memory, amyloidosis
Databáze: OpenAIRE
Externí odkaz: