Modelo de encefalopatia hepática induzida por tioacetamida em camundongos C57BL/6: Estudo comportamental e neuroquímico

Aline Silva de Miranda; David Henrique Rodrigues; Luciene Bruno Vieira; Cristiano Xavier Lima; Milene Alvarenga Rachid; Paula Vieira Teixeira Vidigal; Marcus Vinicius Gomez; Helton José dos Reis; Cristina Guatimosim; Antônio Lúcio Teixeira

doi:10.1590/s0004-282x2010000400022

Modelo de encefalopatia hepática induzida por tioacetamida em camundongos C57BL/6: Estudo comportamental e neuroquímico

Translated title of the contribution: A thioacetamide-induced hepatic encephalopathy model in C57BL/6 mice: A behavioral and neurochemical study

Aline Silva de Miranda, David Henrique Rodrigues, Luciene Bruno Vieira, Cristiano Xavier Lima, Milene Alvarenga Rachid, Paula Vieira Teixeira Vidigal, Marcus Vinicius Gomez, Helton José dos Reis, Cristina Guatimosim, Antônio Lúcio Teixeira

Research output: Contribution to journal › Article › peer-review

26 Scopus citations

Abstract

Objective: Hepatic encephalopathy (HE) is a neuropsychiatric syndrome resulting from liver failure. In the present study, we aimed to standardize an animal model of HE induced by thioacetamide (TAA) in C57BL/6 mice evaluating behavioral symptoms in association with liver damage and alterations in neurotransmitter release. Method: HE was induced by an intraperitoneal single dose of TAA (200 mg/kg, 600 mg/kg or 1,200 mg/kg). Behavioral symptoms were evaluated using the SHIRPA battery. Liver damage was confirmed by histopathological analysis. The glutamate release was measured using fluorimetric assay. Results: The neuropsychiatric state, motor behavior and reflex and sensory functions were significantly altered in the group receiving 600 mg/kg of TAA. Biochemical analysis revealed an increase in the glutamate release in the cerebral cortex of HE mice. Conclusion: HE induced by 600mg/kg TAA injection in C57BL/6 mice seems to be a suitable model to investigate the pathogenesis and clinical disorders of HE.

Translated title of the contribution	A thioacetamide-induced hepatic encephalopathy model in C57BL/6 mice: A behavioral and neurochemical study
Original language	Portuguese
Pages (from-to)	597-602
Number of pages	6
Journal	Arquivos de neuro-psiquiatria
Volume	68
Issue number	4
DOIs	https://doi.org/10.1590/s0004-282x2010000400022
State	Published - Aug 2010
Externally published	Yes

Keywords

Behavioral changes
Glutamate
Hepatic encephalopathy
SHIRPA
Thioacetamide

ASJC Scopus subject areas

Clinical Neurology
Biological Psychiatry

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10.1590/s0004-282x2010000400022

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de Miranda, A. S., Rodrigues, D. H., Vieira, L. B., Lima, C. X., Rachid, M. A., Vidigal, P. V. T., Gomez, M. V., dos Reis, H. J., Guatimosim, C., & Teixeira, A. L. (2010). Modelo de encefalopatia hepática induzida por tioacetamida em camundongos C57BL/6: Estudo comportamental e neuroquímico. Arquivos de neuro-psiquiatria, 68(4), 597-602. https://doi.org/10.1590/s0004-282x2010000400022

de Miranda, AS, Rodrigues, DH, Vieira, LB, Lima, CX, Rachid, MA, Vidigal, PVT, Gomez, MV, dos Reis, HJ, Guatimosim, C & Teixeira, AL 2010, 'Modelo de encefalopatia hepática induzida por tioacetamida em camundongos C57BL/6: Estudo comportamental e neuroquímico', Arquivos de neuro-psiquiatria, vol. 68, no. 4, pp. 597-602. https://doi.org/10.1590/s0004-282x2010000400022

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abstract = "Objective: Hepatic encephalopathy (HE) is a neuropsychiatric syndrome resulting from liver failure. In the present study, we aimed to standardize an animal model of HE induced by thioacetamide (TAA) in C57BL/6 mice evaluating behavioral symptoms in association with liver damage and alterations in neurotransmitter release. Method: HE was induced by an intraperitoneal single dose of TAA (200 mg/kg, 600 mg/kg or 1,200 mg/kg). Behavioral symptoms were evaluated using the SHIRPA battery. Liver damage was confirmed by histopathological analysis. The glutamate release was measured using fluorimetric assay. Results: The neuropsychiatric state, motor behavior and reflex and sensory functions were significantly altered in the group receiving 600 mg/kg of TAA. Biochemical analysis revealed an increase in the glutamate release in the cerebral cortex of HE mice. Conclusion: HE induced by 600mg/kg TAA injection in C57BL/6 mice seems to be a suitable model to investigate the pathogenesis and clinical disorders of HE.",

keywords = "Behavioral changes, Glutamate, Hepatic encephalopathy, SHIRPA, Thioacetamide",

author = "{de Miranda}, {Aline Silva} and Rodrigues, {David Henrique} and Vieira, {Luciene Bruno} and Lima, {Cristiano Xavier} and Rachid, {Milene Alvarenga} and Vidigal, {Paula Vieira Teixeira} and Gomez, {Marcus Vinicius} and {dos Reis}, {Helton Jos{\'e}} and Cristina Guatimosim and Teixeira, {Ant{\^o}nio L{\'u}cio}",

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doi = "10.1590/s0004-282x2010000400022",

language = "Portuguese",

volume = "68",

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AU - Rodrigues, David Henrique

AU - Vieira, Luciene Bruno

AU - Lima, Cristiano Xavier

AU - Rachid, Milene Alvarenga

AU - Vidigal, Paula Vieira Teixeira

AU - Gomez, Marcus Vinicius

AU - dos Reis, Helton José

AU - Guatimosim, Cristina

AU - Teixeira, Antônio Lúcio

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N2 - Objective: Hepatic encephalopathy (HE) is a neuropsychiatric syndrome resulting from liver failure. In the present study, we aimed to standardize an animal model of HE induced by thioacetamide (TAA) in C57BL/6 mice evaluating behavioral symptoms in association with liver damage and alterations in neurotransmitter release. Method: HE was induced by an intraperitoneal single dose of TAA (200 mg/kg, 600 mg/kg or 1,200 mg/kg). Behavioral symptoms were evaluated using the SHIRPA battery. Liver damage was confirmed by histopathological analysis. The glutamate release was measured using fluorimetric assay. Results: The neuropsychiatric state, motor behavior and reflex and sensory functions were significantly altered in the group receiving 600 mg/kg of TAA. Biochemical analysis revealed an increase in the glutamate release in the cerebral cortex of HE mice. Conclusion: HE induced by 600mg/kg TAA injection in C57BL/6 mice seems to be a suitable model to investigate the pathogenesis and clinical disorders of HE.

AB - Objective: Hepatic encephalopathy (HE) is a neuropsychiatric syndrome resulting from liver failure. In the present study, we aimed to standardize an animal model of HE induced by thioacetamide (TAA) in C57BL/6 mice evaluating behavioral symptoms in association with liver damage and alterations in neurotransmitter release. Method: HE was induced by an intraperitoneal single dose of TAA (200 mg/kg, 600 mg/kg or 1,200 mg/kg). Behavioral symptoms were evaluated using the SHIRPA battery. Liver damage was confirmed by histopathological analysis. The glutamate release was measured using fluorimetric assay. Results: The neuropsychiatric state, motor behavior and reflex and sensory functions were significantly altered in the group receiving 600 mg/kg of TAA. Biochemical analysis revealed an increase in the glutamate release in the cerebral cortex of HE mice. Conclusion: HE induced by 600mg/kg TAA injection in C57BL/6 mice seems to be a suitable model to investigate the pathogenesis and clinical disorders of HE.

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Modelo de encefalopatia hepática induzida por tioacetamida em camundongos C57BL/6: Estudo comportamental e neuroquímico

Abstract

Keywords

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