Attenuating effect of chlorella supplementation on oxidative stress and NFκB activation in peritoneal macrophages and liver of C57BL/6 mice fed on an atherogenic diet
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作者:
Lee, HS
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机构:Inje Univ, Sch Food & Life Sci, Kimhae 621749, South Korea
Lee, HS
Choi, CY
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机构:Inje Univ, Sch Food & Life Sci, Kimhae 621749, South Korea
Choi, CY
Cho, C
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机构:Inje Univ, Sch Food & Life Sci, Kimhae 621749, South Korea
Cho, C
Song, Y
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机构:Inje Univ, Sch Food & Life Sci, Kimhae 621749, South Korea
Song, Y
机构:
[1] Inje Univ, Sch Food & Life Sci, Kimhae 621749, South Korea
[2] Inje Univ, Biohlth Prod Res Ctr, Kimhae 621749, South Korea
[3] Inje Univ, Sch Biomed & Biotechnol, Kimhae, South Korea
This study was designed to investigate whether chlorella supplementation may ameliorate oxidative stress and nuclear factor kappa B (NFkappaB) activation in peritoneal macrophages and liver of C57BL/6 mice fed on an atherogenic diet. The animals were maintained on an atherogenic diet (control), or an atherogenic diet supplemented with 3% (w/w) chlorella or 5% (w/w) chlorella for 12 wks. The plasma and hepatic lipid levels were not affected by chlorella supplementation. Hepatic thiobarbituric acid-reactive substances and superoxide anion production in peritoneal macrophages were significantly lower in the 5 % chlorella group (p<0.05), but the glutathione level was not altered by chlorella supplementation. The hepatic antioxidative enzyme activities of Cu, Zn-superoxide dismutase and catalase were higher in the mice fed on the 5% chlorella diet (p<0.05). The plasma aspartate aminotransferase activity was lower in the mice fed on the chlorella-containing diets (p<0.05), whereas the alanine aminotransferase activity was not affected by chlorella supplementation. The NFkappaB nuclear binding activities of peritoneal macrophages and liver were significantly lower in the 5 % chlorella groups (p<0.05). These results suggest that chlorella supplementation may attenuate oxidative stress by reducing reactive oxygen production and increasing antioxidative processes, thus suppressing inflammatory mediator activation in peritoneal macrophages and liver.
机构:
San Diego State Univ, Mammalian Cell & Mol Biol Lab, San Diego, CA 92182 USASan Diego State Univ, Mammalian Cell & Mol Biol Lab, San Diego, CA 92182 USA
Davis, RA
;
Hui, TY
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机构:
San Diego State Univ, Mammalian Cell & Mol Biol Lab, San Diego, CA 92182 USASan Diego State Univ, Mammalian Cell & Mol Biol Lab, San Diego, CA 92182 USA
机构:
San Diego State Univ, Mammalian Cell & Mol Biol Lab, San Diego, CA 92182 USASan Diego State Univ, Mammalian Cell & Mol Biol Lab, San Diego, CA 92182 USA
Davis, RA
;
Hui, TY
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机构:
San Diego State Univ, Mammalian Cell & Mol Biol Lab, San Diego, CA 92182 USASan Diego State Univ, Mammalian Cell & Mol Biol Lab, San Diego, CA 92182 USA