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.
Article
em En
| WPRIM
| ID: wpr-51348
Biblioteca responsável:
WPRO
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.
Palavras-chave
Texto completo:
1
Índice:
WPRIM
Assunto principal:
Vitamina E
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Vitaminas
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Linfócitos
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Peroxidação de Lipídeos
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Linfócitos T Auxiliares-Indutores
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Micronutrientes
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Dieta
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Mortalidade Prematura
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Mitógenos
Tipo de estudo:
Diagnostic_studies
Limite:
Animals
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Female
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Humans
Idioma:
En
Revista:
Nutrition Research and Practice
Ano de publicação:
2014
Tipo de documento:
Article