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Provedor de dados: |
BJMBR
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País: |
Brazil
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Título: |
Galantamine protects against lipopolysaccharide-induced acute lung injury in rats
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Autores: |
Li,G.
Zhou,CL.
Zhou,QS.
Zou,HD.
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Data: |
2016-01-01
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Ano: |
2016
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Palavras-chave: |
Galantamine
Acute lung injury
Lipopolysaccharide
HMGB1
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Resumo: |
Lipopolysaccharide (LPS)-induced endotoxemia triggers the secretion of proinflammatory cytokines and can cause acute lung injury (ALI). The high mobility group box 1 (HMGB1) protein plays an important role as a late mediator of sepsis and ALI. Galantamine (GAL) is a central acetylcholinesterase inhibitor that inhibits the expression of HMGB1. This study evaluated the effects of GAL by measuring levels of inflammatory mediators and observing histopathological features associated with LPS-induced ALI. Sixty 8-10 week old male Sprague-Dawley rats (200-240 g) were randomized into three groups as follows: control group, LPS group (7.5 mg/kg LPS), and LPS+GAL group (5 mg/kg GAL before LPS administration). Histopathological examination of lung specimens obtained 12 h after LPS administration was performed to analyze changes in wet-to-dry (W/D) weight ratio, myeloperoxidase (MPO) activity, and HMGB1 expression level. Additionally, plasma concentrations of tumor necrosis factor-α, interleukin-6, and HMGB1 were measured using an enzyme-linked immunosorbent assay at 0 (baseline), 3, 6, 9, and 12 h after LPS administration. Mortality in the three groups was recorded at 72 h. LPS-induced ALI was characterized by distortion of pulmonary architecture and elevation of MPO activity, W/D weight ratio, and levels of pro-inflammatory cytokines, including tumor necrosis factor-α, interleukin-6, and HMGB1. Pretreatment with GAL significantly reduced the LPS-induced lung pathological changes, W/D weight ratio, levels of pro-inflammatory cytokines and MPO activity (ANOVA). Moreover, GAL treatment significantly decreased the mortality rate (ANOVA). In conclusion, we demonstrated that GAL exerted a protective effect on LPS-induced ALI in rats.
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Tipo: |
Info:eu-repo/semantics/article
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Idioma: |
Inglês
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Identificador: |
http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2016000200601
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Editor: |
Associação Brasileira de Divulgação Científica
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Relação: |
10.1590/1414-431x20155008
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Formato: |
text/html
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Fonte: |
Brazilian Journal of Medical and Biological Research v.49 n.2 2016
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Direitos: |
info:eu-repo/semantics/openAccess
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