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Inosine protects against impairment of memory induced by experimental model of Alzheimer disease: a nucleoside with multitarget brain actions.
Psychopharmacology (Berl). 2020 Mar; 237(3):811-823.P

Abstract

RATIONALE

Inosine is a naturally occurring purine nucleoside formed by adenosine breakdown. This nucleoside is reported to exert potent effects on memory and learning, possibly through its antioxidant and anti-inflammatory actions.

OBJECTIVE

The objective is to evaluate the effects of inosine on the behavioral and neurochemical parameters in a rat model of Alzheimer's disease (AD) induced by streptozotocin (STZ).

METHODS

Adult male rats were divided into four groups: control (saline), STZ, STZ plus inosine (50 mg/kg), and STZ plus inosine (100 mg/kg). STZ (3 mg/kg) was administered by bilateral intracerebroventricular injection. The animals were treated intraperitoneally with inosine for 25 days. Memory, oxidative stress, ion pump activities, acetylcholinesterase (AChE), and choline acetyltransferase (ChAT) activities and expression were evaluated in the cerebral cortex and hippocampus.

RESULTS

The memory impairment induced by STZ was prevented by inosine. An increase in the Na+, K+-ATPase, and Mg-ATPase activities and a decrease in the Ca2+-ATPase activity were induced by STZ in the hippocampus and cerebral cortex, and inosine could prevent these alterations in ion pump activities. Inosine also prevented the increase in AChE activity and the alterations in AChE and ChAT expression induced by STZ. STZ increased the reactive oxygen species, nitrite levels, and superoxide dismutase activity and decreased the catalase and glutathione peroxidase activities. Inosine treatment conferred protection from these oxidative alterations in the brain.

CONCLUSIONS

Our findings demonstrate that inosine affects brain multiple targets suggesting that this molecule may have therapeutic potential against cognitive deficit and tissue damage in AD.

Authors+Show Affiliations

Programa de Pós-Graduação em Bioquímica e Bioprospecção, Centro de Ciências Químicas, Farmacêuticas e de Alimentos, Universidade Federal de Pelotas, Campus Universitário S/N, Pelotas, RS, Brazil.Programa de Pós-Graduação em Patologia, Laboratório de Pesquisa em Patologia, Universidade Federal de Ciências da Saúde de Porto Alegre, Porto Alegre, RS, Brazil.Programa de Pós-Graduação em Bioquímica e Bioprospecção, Centro de Ciências Químicas, Farmacêuticas e de Alimentos, Universidade Federal de Pelotas, Campus Universitário S/N, Pelotas, RS, Brazil.Programa de Pós-Graduação em Bioquímica e Bioprospecção, Centro de Ciências Químicas, Farmacêuticas e de Alimentos, Universidade Federal de Pelotas, Campus Universitário S/N, Pelotas, RS, Brazil.Programa de Pós-Graduação em Bioquímica e Bioprospecção, Centro de Ciências Químicas, Farmacêuticas e de Alimentos, Universidade Federal de Pelotas, Campus Universitário S/N, Pelotas, RS, Brazil.Programa de Pós-Graduação em Bioquímica e Bioprospecção, Centro de Ciências Químicas, Farmacêuticas e de Alimentos, Universidade Federal de Pelotas, Campus Universitário S/N, Pelotas, RS, Brazil.Programa de Pós-Graduação em Bioquímica e Bioprospecção, Centro de Ciências Químicas, Farmacêuticas e de Alimentos, Universidade Federal de Pelotas, Campus Universitário S/N, Pelotas, RS, Brazil.Programa de Pós-Graduação em Bioquímica Toxicológica, Departamento de Bioquímica e Biologia Molecular, Centro de Ciências Naturais e Exatas, Universidade Federal de Santa Maria, Santa Maria, RS, Brazil.Programa de Pós-Graduação em Bioquímica Toxicológica, Departamento de Bioquímica e Biologia Molecular, Centro de Ciências Naturais e Exatas, Universidade Federal de Santa Maria, Santa Maria, RS, Brazil.Programa de Pós-Graduação em Farmacologia, Departamento de Fisiologia e Farmacologia, Centro de Ciências da Saúde, Universidade Federal de Santa Maria, Santa Maria, RS, Brazil.Programa de Pós-Graduação em Bioquímica e Bioprospecção, Centro de Ciências Químicas, Farmacêuticas e de Alimentos, Universidade Federal de Pelotas, Campus Universitário S/N, Pelotas, RS, Brazil.Programa de Pós-Graduação em Bioquímica e Bioprospecção, Centro de Ciências Químicas, Farmacêuticas e de Alimentos, Universidade Federal de Pelotas, Campus Universitário S/N, Pelotas, RS, Brazil. rspanevello@gmail.com. Programa de Pós-Graduação em Bioquímica e Bioprospecção, Laboratório de Neuroquímica, Inflamação e Câncer, Centro de Ciências Químicas, Farmacêuticas e de Alimentos, Universidade Federal de Pelotas, Campus Universitário, Capão do Leão, Pelotas, RS, 96010-900, Brazil. rspanevello@gmail.com.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

31834453

Citation

Teixeira, Fernanda Cardoso, et al. "Inosine Protects Against Impairment of Memory Induced By Experimental Model of Alzheimer Disease: a Nucleoside With Multitarget Brain Actions." Psychopharmacology, vol. 237, no. 3, 2020, pp. 811-823.
Teixeira FC, Gutierres JM, Soares MSP, et al. Inosine protects against impairment of memory induced by experimental model of Alzheimer disease: a nucleoside with multitarget brain actions. Psychopharmacology (Berl). 2020;237(3):811-823.
Teixeira, F. C., Gutierres, J. M., Soares, M. S. P., da Siveira de Mattos, B., Spohr, L., do Couto, C. A. T., Bona, N. P., Assmann, C. E., Morsch, V. M., da Cruz, I. B. M., Stefanello, F. M., & Spanevello, R. M. (2020). Inosine protects against impairment of memory induced by experimental model of Alzheimer disease: a nucleoside with multitarget brain actions. Psychopharmacology, 237(3), 811-823. https://doi.org/10.1007/s00213-019-05419-5
Teixeira FC, et al. Inosine Protects Against Impairment of Memory Induced By Experimental Model of Alzheimer Disease: a Nucleoside With Multitarget Brain Actions. Psychopharmacology (Berl). 2020;237(3):811-823. PubMed PMID: 31834453.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Inosine protects against impairment of memory induced by experimental model of Alzheimer disease: a nucleoside with multitarget brain actions. AU - Teixeira,Fernanda Cardoso, AU - Gutierres,Jessié Martins, AU - Soares,Mayara Sandrielly Pereira, AU - da Siveira de Mattos,Bruna, AU - Spohr,Luiza, AU - do Couto,Carlus Augustu Tavares, AU - Bona,Natália Pontes, AU - Assmann,Charles Elias, AU - Morsch,Vera Maria, AU - da Cruz,Ivana Beatrice Mânica, AU - Stefanello,Francieli Moro, AU - Spanevello,Roselia Maria, Y1 - 2019/12/13/ PY - 2019/05/01/received PY - 2019/11/27/accepted PY - 2019/12/14/pubmed PY - 2020/8/12/medline PY - 2019/12/14/entrez KW - Acetylcholinesterase KW - Alzheimer’s disease KW - Brain KW - Inosine KW - Na+, K+-ATPase KW - Oxidative stress SP - 811 EP - 823 JF - Psychopharmacology JO - Psychopharmacology (Berl) VL - 237 IS - 3 N2 - RATIONALE: Inosine is a naturally occurring purine nucleoside formed by adenosine breakdown. This nucleoside is reported to exert potent effects on memory and learning, possibly through its antioxidant and anti-inflammatory actions. OBJECTIVE: The objective is to evaluate the effects of inosine on the behavioral and neurochemical parameters in a rat model of Alzheimer's disease (AD) induced by streptozotocin (STZ). METHODS: Adult male rats were divided into four groups: control (saline), STZ, STZ plus inosine (50 mg/kg), and STZ plus inosine (100 mg/kg). STZ (3 mg/kg) was administered by bilateral intracerebroventricular injection. The animals were treated intraperitoneally with inosine for 25 days. Memory, oxidative stress, ion pump activities, acetylcholinesterase (AChE), and choline acetyltransferase (ChAT) activities and expression were evaluated in the cerebral cortex and hippocampus. RESULTS: The memory impairment induced by STZ was prevented by inosine. An increase in the Na+, K+-ATPase, and Mg-ATPase activities and a decrease in the Ca2+-ATPase activity were induced by STZ in the hippocampus and cerebral cortex, and inosine could prevent these alterations in ion pump activities. Inosine also prevented the increase in AChE activity and the alterations in AChE and ChAT expression induced by STZ. STZ increased the reactive oxygen species, nitrite levels, and superoxide dismutase activity and decreased the catalase and glutathione peroxidase activities. Inosine treatment conferred protection from these oxidative alterations in the brain. CONCLUSIONS: Our findings demonstrate that inosine affects brain multiple targets suggesting that this molecule may have therapeutic potential against cognitive deficit and tissue damage in AD. SN - 1432-2072 UR - https://www.unboundmedicine.com/medline/citation/31834453/Inosine_protects_against_impairment_of_memory_induced_by_experimental_model_of_Alzheimer_disease:_a_nucleoside_with_multitarget_brain_actions_ L2 - https://dx.doi.org/10.1007/s00213-019-05419-5 DB - PRIME DP - Unbound Medicine ER -