Pycnogenol attenuates the symptoms of immune dysfunction through restoring a cellular antioxidant status in low micronutrient-induced immune deficient mice
Nutrition Research and Practice
;
: 533-538, 2014.
Artigo
em Inglês
| WPRIM
| ID: wpr-51348
ABSTRACT
BACKGROUND/OBJECTIVES:
We investigated the effect of Pycnogenol (Pyc) on survival and immune dysfunction of C57BL/6 mice induced by low micronutrient supplementation. MATERIALS/METHODS:
Female C57/BL/6 mice were fed a diet containing 7.5% of the recommended amount of micronutrients for a period of 12 wks (immunological assay) and 18 wks (survival test). For immunological assay, lymphocyte proliferation, cytokine regulation, and hepatic oxidative status were determined. RESLUTS Pyc supplementation with 50 and 100 mg.kg(-1).bw.d(-1) resulted in partial extension of the median survival time. Pyc supplementation led to increased T and B cell response against mitogens and recovery of an abnormal shift of cytokine pattern designated by the decreased secretion of Th1 cytokine and increased secretion of Th2 cytokine. Hepatic vitamin E level was significantly decreased by micronutrient deficiency, in accordance with increased hepatic lipid peroxidation level. However, Pyc supplementation resulted in a dose-dependent reduction of hepatic lipid peroxidation, which may result from restoration of hepatic vitamin E level.CONCLUSION:
Findings of this study suggest that Pyc supplementation ameliorates premature death by restoring immune dysfunction, such as increasing lymphocyte proliferation and regulation of cytokine release from helper T cells, which may result from the antioxidative ability of Pyc.
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Vitamina E
/
Vitaminas
/
Linfócitos
/
Peroxidação de Lipídeos
/
Linfócitos T Auxiliares-Indutores
/
Micronutrientes
/
Dieta
/
Mortalidade Prematura
/
Mitógenos
Tipo de estudo:
Estudo diagnóstico
Limite:
Animais
/
Feminino
/
Humanos
Idioma:
Inglês
Revista:
Nutrition Research and Practice
Ano de publicação:
2014
Tipo de documento:
Artigo
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