Repression of proinflammatory gene expression by lipid extract of Nostoc commune var sphaeroides Kützing, a blue-green alga, via inhibition of nuclear factor-κB in RAW 264.7 macrophages

Young Ki Park, Heather E. Rasmussen, Sarah J. Ehlers, Kara R. Blobaum, Fan Lu, Vicki L. Schlegal, Timothy P. Carr, Ji Young Lee

Research output: Contribution to journalArticle

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Abstract

We investigated whether lipid extract from a blue-green alga, N commune, modulates proinflammatory gene expression in RAW 264.7 macrophages. The cells were incubated with N commune lipid extract (0-100 μg/mL) and subsequently activated by LPS (100 ng/mL). Quantitative real-time PCR analysis showed that mRNA abundance of proinflammatory mediators, including TNF-α, COX-2, IL-1β, IL-6, and iNOS, was significantly reduced by N commune lipid extract in a dose-dependent manner. Secretion of TNF-α and IL-1β into cell culture medium was also significantly decreased by N commune lipid extract. Thin-layer chromatography-densitometry analysis showed that N commune lipid extract contained approximately 15% of fatty acids. To determine whether the inhibition of proinflammatory mediator production by N commune lipid extract is primarily conferred by fatty acids in the lipid extract, macrophages were incubated with 100 μg/mL of N commune lipid extract or 15 μg/mL of a fatty acid mixture, which was formulated to reflect the fatty acid composition of N commune lipid extract. The fatty acid mixture significantly reduced RNA abundance of TNF-α and COX-2, but to a lesser extent than did the N commune lipid extract, suggesting the presence of additional bioactive compounds with an antiinflammatory property in the lipid extract. As NF-κB is a major regulator for the proinflammatory gene expression, we measured its DNA-binding activity. DNA-binding activity of NF-κB was significantly reduced by N commune lipid extract. In conclusion, our study suggests that N commune lipid extract represses the expression of proinflammatory genes in RAW 264.7 macrophages, at least in part, by inhibiting the activation of NF-κB pathway.

Original languageEnglish (US)
Pages (from-to)83-91
Number of pages9
JournalNutrition Research
Volume28
Issue number2
DOIs
StatePublished - Feb 1 2008

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Nostoc commune
Cyanobacteria
Macrophages
Lipids
Gene Expression
Fatty Acids
Interleukin-1

Keywords

  • Antiinflammatory
  • Blue-green algae
  • COX-2
  • IL-1β
  • IL-6
  • LPS
  • N. commune
  • NF-κB
  • Nostoc commune var sphaeroides
  • Nostoc commune var sphaeroides Kützing
  • RAW 264.7 macrophages
  • TNF-α
  • cyclooxygenase 2
  • iNOS
  • inducible nitric oxide synthase
  • interleukin-1β
  • interleukin-6
  • lipopolysaccharide
  • nuclear factor-kappa B
  • tumor necrosis factor-α

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology
  • Nutrition and Dietetics

Cite this

Repression of proinflammatory gene expression by lipid extract of Nostoc commune var sphaeroides Kützing, a blue-green alga, via inhibition of nuclear factor-κB in RAW 264.7 macrophages. / Park, Young Ki; Rasmussen, Heather E.; Ehlers, Sarah J.; Blobaum, Kara R.; Lu, Fan; Schlegal, Vicki L.; Carr, Timothy P.; Lee, Ji Young.

In: Nutrition Research, Vol. 28, No. 2, 01.02.2008, p. 83-91.

Research output: Contribution to journalArticle

Park, Young Ki ; Rasmussen, Heather E. ; Ehlers, Sarah J. ; Blobaum, Kara R. ; Lu, Fan ; Schlegal, Vicki L. ; Carr, Timothy P. ; Lee, Ji Young. / Repression of proinflammatory gene expression by lipid extract of Nostoc commune var sphaeroides Kützing, a blue-green alga, via inhibition of nuclear factor-κB in RAW 264.7 macrophages. In: Nutrition Research. 2008 ; Vol. 28, No. 2. pp. 83-91.
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abstract = "We investigated whether lipid extract from a blue-green alga, N commune, modulates proinflammatory gene expression in RAW 264.7 macrophages. The cells were incubated with N commune lipid extract (0-100 μg/mL) and subsequently activated by LPS (100 ng/mL). Quantitative real-time PCR analysis showed that mRNA abundance of proinflammatory mediators, including TNF-α, COX-2, IL-1β, IL-6, and iNOS, was significantly reduced by N commune lipid extract in a dose-dependent manner. Secretion of TNF-α and IL-1β into cell culture medium was also significantly decreased by N commune lipid extract. Thin-layer chromatography-densitometry analysis showed that N commune lipid extract contained approximately 15{\%} of fatty acids. To determine whether the inhibition of proinflammatory mediator production by N commune lipid extract is primarily conferred by fatty acids in the lipid extract, macrophages were incubated with 100 μg/mL of N commune lipid extract or 15 μg/mL of a fatty acid mixture, which was formulated to reflect the fatty acid composition of N commune lipid extract. The fatty acid mixture significantly reduced RNA abundance of TNF-α and COX-2, but to a lesser extent than did the N commune lipid extract, suggesting the presence of additional bioactive compounds with an antiinflammatory property in the lipid extract. As NF-κB is a major regulator for the proinflammatory gene expression, we measured its DNA-binding activity. DNA-binding activity of NF-κB was significantly reduced by N commune lipid extract. In conclusion, our study suggests that N commune lipid extract represses the expression of proinflammatory genes in RAW 264.7 macrophages, at least in part, by inhibiting the activation of NF-κB pathway.",
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author = "Park, {Young Ki} and Rasmussen, {Heather E.} and Ehlers, {Sarah J.} and Blobaum, {Kara R.} and Fan Lu and Schlegal, {Vicki L.} and Carr, {Timothy P.} and Lee, {Ji Young}",
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AU - Park, Young Ki

AU - Rasmussen, Heather E.

AU - Ehlers, Sarah J.

AU - Blobaum, Kara R.

AU - Lu, Fan

AU - Schlegal, Vicki L.

AU - Carr, Timothy P.

AU - Lee, Ji Young

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N2 - We investigated whether lipid extract from a blue-green alga, N commune, modulates proinflammatory gene expression in RAW 264.7 macrophages. The cells were incubated with N commune lipid extract (0-100 μg/mL) and subsequently activated by LPS (100 ng/mL). Quantitative real-time PCR analysis showed that mRNA abundance of proinflammatory mediators, including TNF-α, COX-2, IL-1β, IL-6, and iNOS, was significantly reduced by N commune lipid extract in a dose-dependent manner. Secretion of TNF-α and IL-1β into cell culture medium was also significantly decreased by N commune lipid extract. Thin-layer chromatography-densitometry analysis showed that N commune lipid extract contained approximately 15% of fatty acids. To determine whether the inhibition of proinflammatory mediator production by N commune lipid extract is primarily conferred by fatty acids in the lipid extract, macrophages were incubated with 100 μg/mL of N commune lipid extract or 15 μg/mL of a fatty acid mixture, which was formulated to reflect the fatty acid composition of N commune lipid extract. The fatty acid mixture significantly reduced RNA abundance of TNF-α and COX-2, but to a lesser extent than did the N commune lipid extract, suggesting the presence of additional bioactive compounds with an antiinflammatory property in the lipid extract. As NF-κB is a major regulator for the proinflammatory gene expression, we measured its DNA-binding activity. DNA-binding activity of NF-κB was significantly reduced by N commune lipid extract. In conclusion, our study suggests that N commune lipid extract represses the expression of proinflammatory genes in RAW 264.7 macrophages, at least in part, by inhibiting the activation of NF-κB pathway.

AB - We investigated whether lipid extract from a blue-green alga, N commune, modulates proinflammatory gene expression in RAW 264.7 macrophages. The cells were incubated with N commune lipid extract (0-100 μg/mL) and subsequently activated by LPS (100 ng/mL). Quantitative real-time PCR analysis showed that mRNA abundance of proinflammatory mediators, including TNF-α, COX-2, IL-1β, IL-6, and iNOS, was significantly reduced by N commune lipid extract in a dose-dependent manner. Secretion of TNF-α and IL-1β into cell culture medium was also significantly decreased by N commune lipid extract. Thin-layer chromatography-densitometry analysis showed that N commune lipid extract contained approximately 15% of fatty acids. To determine whether the inhibition of proinflammatory mediator production by N commune lipid extract is primarily conferred by fatty acids in the lipid extract, macrophages were incubated with 100 μg/mL of N commune lipid extract or 15 μg/mL of a fatty acid mixture, which was formulated to reflect the fatty acid composition of N commune lipid extract. The fatty acid mixture significantly reduced RNA abundance of TNF-α and COX-2, but to a lesser extent than did the N commune lipid extract, suggesting the presence of additional bioactive compounds with an antiinflammatory property in the lipid extract. As NF-κB is a major regulator for the proinflammatory gene expression, we measured its DNA-binding activity. DNA-binding activity of NF-κB was significantly reduced by N commune lipid extract. In conclusion, our study suggests that N commune lipid extract represses the expression of proinflammatory genes in RAW 264.7 macrophages, at least in part, by inhibiting the activation of NF-κB pathway.

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KW - cyclooxygenase 2

KW - iNOS

KW - inducible nitric oxide synthase

KW - interleukin-1β

KW - interleukin-6

KW - lipopolysaccharide

KW - nuclear factor-kappa B

KW - tumor necrosis factor-α

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