Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 2 de 2
Filter
Add more filters










Database
Language
Publication year range
1.
Br J Nutr ; 101(8): 1246-54, 2009 Apr.
Article in English | MEDLINE | ID: mdl-19243638

ABSTRACT

The present study was undertaken to assess the beneficial effects of a daily consumption of 8 % freeze-dried red-pigmented leafy lettuce (Lactuca sativa) on CVD. C57BL/6J mice were fed a high-fat high-cholesterol diet supplemented with or without red-pigmented leafy lettuce for 4 weeks. The present results showed that the red-pigmented leafy lettuce-supplemented diet significantly decreased the level of total and LDL-cholesterol and TAG in the plasma of the mice. The atherosclerotic index was calculated to be 46 % lower in the mice fed with the lettuce diet compared with the control diet. Lipid peroxidation measured by 2-thiobarbituric acid-reactive substances was markedly reduced in the plasma, liver, heart and kidney of the mice fed the lettuce diet. The content of antioxidants (total glutathione and beta-carotene) was significantly increased by lettuce supplementation. The antioxidant defence system by antioxidant enzymes including glutathione S-transferase, glutathione peroxidase, glutathione reductase, superoxide dismutase and paraoxanase in blood or liver tissues was also increased, and showed the improved oxidative stress in the mice fed the lettuce diet. The measurement of tail DNA (%), tail extent moment and olive tail moment indicated that the lettuce diet increased the resistance of hepatocyte and lymphocyte DNA to oxidative damage. The present study showed that the supplementation of a high-cholesterol high-fat diet with 8 % red-pigmented leafy lettuce resulted in an improvement of plasma cholesterol and lipid levels, prevention of lipid peroxidation and an increase of the antioxidant defence system and, therefore, could contribute to reduce the risk factors of CVD.


Subject(s)
Antioxidants/metabolism , Dietary Fats/administration & dosage , Dietary Supplements , Lactuca/chemistry , Lipid Peroxidation/physiology , Animals , Body Weight/physiology , Cholesterol, Dietary/administration & dosage , DNA Damage , Diet , Eating/physiology , Feces/chemistry , Hepatocytes/metabolism , Male , Mice , Mice, Inbred C57BL , Oxidative Stress/physiology , Pigments, Biological/analysis
2.
Int J Neurosci ; 117(7): 885-94, 2007 Jul.
Article in English | MEDLINE | ID: mdl-17613102

ABSTRACT

Microglial cells are thought to be major inflammatory cells in the central nervous system; however, sufficient information about the effects of double-stranded RNA (dsRNA) in microglial cells is lacking. The present study compared the innate immune responses of the murine microglial cell line BV2 to dsRNA and lipopolysaccharide (LPS). It showed that the effect of dsRNA was similar to that of LPS treatment. The dsRNA induced several pro-inflammatory factors such as TNF-alpha, IL-6, IL-1beta, and IL-1Ra. Furthermore, the expression level of COX-2 was increased after treatment with dsRNA. However, the induction level of IL-1beta by dsRNA was less than those of the other cytokines that were measured. These results suggest that, although both dsRNA and LPS trigger pro-inflammatory responses, the intracellular signaling pathway and inflammation pattern of dsRNA and LPS may be different. Therefore, dsRNA produced during viral infection could precipitate neurological abnormalities through chronic inflammation.


Subject(s)
Immunity, Innate/immunology , Inflammation Mediators/metabolism , Lipopolysaccharides/immunology , Microglia/immunology , Poly I-C/immunology , Animals , Cell Line , Cyclooxygenase 2/genetics , Cyclooxygenase 2/metabolism , Gene Expression Regulation/immunology , Immunity, Innate/physiology , Interleukin 1 Receptor Antagonist Protein/genetics , Interleukin 1 Receptor Antagonist Protein/metabolism , Interleukin-1beta/genetics , Interleukin-1beta/metabolism , Interleukin-6/genetics , Interleukin-6/metabolism , Mice , RNA, Double-Stranded/immunology , RNA, Messenger/analysis , Signal Transduction , Tumor Necrosis Factor-alpha/genetics , Tumor Necrosis Factor-alpha/metabolism
SELECTION OF CITATIONS
SEARCH DETAIL
...