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Erucin exerts anti-inflammatory properties in murine macrophages and mouse skin: possible mediation through the inhibition of NFκB signaling.

Cho HJ, Lee KW, Park JH - Int J Mol Sci (2013)

Bottom Line: In RAW 264.7 cells, erucin (2.5, 5 μmol/L) inhibited LPS-induced production of nitric oxide and prostaglandin E2.Erucin inhibited LPS-induced degradation of the inhibitor of κBα and translocation of p65 to the nucleus and, subsequently, reduced LPS-induced nuclear factor κB (NFκB) DNA binding activities, as well as the transcriptional activity of NFκB, leading to the decreased expression of NFκB-target genes, including tumor necrosis factor-α, interleukin (IL)-6, IL-1β, inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2, as well as transcriptional activity of iNOS and COX-2.These results indicate that erucin exerts a potent anti-inflammatory activity by inhibiting the pro-inflammatory enzymes and cytokines, which may be mediated, at least in part, via the inhibition of NFκB signaling.

View Article: PubMed Central - PubMed

Affiliation: Department of Food and Nutrition, Hallym University, Chuncheon 200-702, Korea. jyoon@hallym.ac.kr.

ABSTRACT
Erucin, an isothiocyanate, is a hydrolysis product of glucoerucin found in arugula and has recently been reported to have anti-cancer properties in various cancer cells. In this study, we assessed the anti-inflammatory effects of erucin and the underlying mechanisms, using lipopolysaccharide (LPS)-stimulated RAW 264.7 murine macrophages and 12-O-tetradecanoylphorbol-13-acetate-treated mouse skin. In RAW 264.7 cells, erucin (2.5, 5 μmol/L) inhibited LPS-induced production of nitric oxide and prostaglandin E2. Erucin inhibited LPS-induced degradation of the inhibitor of κBα and translocation of p65 to the nucleus and, subsequently, reduced LPS-induced nuclear factor κB (NFκB) DNA binding activities, as well as the transcriptional activity of NFκB, leading to the decreased expression of NFκB-target genes, including tumor necrosis factor-α, interleukin (IL)-6, IL-1β, inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2, as well as transcriptional activity of iNOS and COX-2. In mice, erucin (100, 300 nmoles) treatment significantly inhibited phorbol ester-induced formation of ear edema and expression of iNOS and COX-2 proteins. These results indicate that erucin exerts a potent anti-inflammatory activity by inhibiting the pro-inflammatory enzymes and cytokines, which may be mediated, at least in part, via the inhibition of NFκB signaling.

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Erucin decreases LPS-induced expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2 in RAW 264.7 cells. RAW 264.7 cells were treated with various concentrations of erucin in the presence of LPS. (A) Cell lysates were subjected to Western blotting with their relevant antibodies. The relative abundance of each band to their own β-actin was quantified, and the LPS control levels were set at 100%. The adjusted mean ± SEM (n = 3) of each band is shown above each blot; (B,C) Total RNA was isolated, and real-time RT-PCR was performed; (D,E) RAW 264.7 cells were transfected with the murine iNOS or COX-2 reporter gene construct. The transfected cells were treated with various concentrations of erucin in the presence of LPS. Cell lysates were prepared to determine luciferase activity. Each bar represents the mean ± SEM (n = 4). Means without a common letter differ (p < 0.05). ND: not detected.
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f2-ijms-14-20564: Erucin decreases LPS-induced expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2 in RAW 264.7 cells. RAW 264.7 cells were treated with various concentrations of erucin in the presence of LPS. (A) Cell lysates were subjected to Western blotting with their relevant antibodies. The relative abundance of each band to their own β-actin was quantified, and the LPS control levels were set at 100%. The adjusted mean ± SEM (n = 3) of each band is shown above each blot; (B,C) Total RNA was isolated, and real-time RT-PCR was performed; (D,E) RAW 264.7 cells were transfected with the murine iNOS or COX-2 reporter gene construct. The transfected cells were treated with various concentrations of erucin in the presence of LPS. Cell lysates were prepared to determine luciferase activity. Each bar represents the mean ± SEM (n = 4). Means without a common letter differ (p < 0.05). ND: not detected.

Mentions: We next investigated whether erucin inhibits the expression of iNOS and COX-2. The results of Western blot analysis revealed that LPS increased the protein expression of iNOS and COX-2, which was decreased by erucin treatment (Figure 2A). The levels of iNOS and COX-2 mRNAs were changed in parallel with those of their corresponding proteins (Figure 2B,C). Erucin treatment significantly inhibited LPS-induced iNOS and COX-2 transcriptional activity (Figure 2D,E). These results indicate that erucin decreases LPS-induced NO and PGE2 production through the downregulation of iNOS and COX-2 expression.


Erucin exerts anti-inflammatory properties in murine macrophages and mouse skin: possible mediation through the inhibition of NFκB signaling.

Cho HJ, Lee KW, Park JH - Int J Mol Sci (2013)

Erucin decreases LPS-induced expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2 in RAW 264.7 cells. RAW 264.7 cells were treated with various concentrations of erucin in the presence of LPS. (A) Cell lysates were subjected to Western blotting with their relevant antibodies. The relative abundance of each band to their own β-actin was quantified, and the LPS control levels were set at 100%. The adjusted mean ± SEM (n = 3) of each band is shown above each blot; (B,C) Total RNA was isolated, and real-time RT-PCR was performed; (D,E) RAW 264.7 cells were transfected with the murine iNOS or COX-2 reporter gene construct. The transfected cells were treated with various concentrations of erucin in the presence of LPS. Cell lysates were prepared to determine luciferase activity. Each bar represents the mean ± SEM (n = 4). Means without a common letter differ (p < 0.05). ND: not detected.
© Copyright Policy - open-access
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC3821631&req=5

f2-ijms-14-20564: Erucin decreases LPS-induced expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2 in RAW 264.7 cells. RAW 264.7 cells were treated with various concentrations of erucin in the presence of LPS. (A) Cell lysates were subjected to Western blotting with their relevant antibodies. The relative abundance of each band to their own β-actin was quantified, and the LPS control levels were set at 100%. The adjusted mean ± SEM (n = 3) of each band is shown above each blot; (B,C) Total RNA was isolated, and real-time RT-PCR was performed; (D,E) RAW 264.7 cells were transfected with the murine iNOS or COX-2 reporter gene construct. The transfected cells were treated with various concentrations of erucin in the presence of LPS. Cell lysates were prepared to determine luciferase activity. Each bar represents the mean ± SEM (n = 4). Means without a common letter differ (p < 0.05). ND: not detected.
Mentions: We next investigated whether erucin inhibits the expression of iNOS and COX-2. The results of Western blot analysis revealed that LPS increased the protein expression of iNOS and COX-2, which was decreased by erucin treatment (Figure 2A). The levels of iNOS and COX-2 mRNAs were changed in parallel with those of their corresponding proteins (Figure 2B,C). Erucin treatment significantly inhibited LPS-induced iNOS and COX-2 transcriptional activity (Figure 2D,E). These results indicate that erucin decreases LPS-induced NO and PGE2 production through the downregulation of iNOS and COX-2 expression.

Bottom Line: In RAW 264.7 cells, erucin (2.5, 5 μmol/L) inhibited LPS-induced production of nitric oxide and prostaglandin E2.Erucin inhibited LPS-induced degradation of the inhibitor of κBα and translocation of p65 to the nucleus and, subsequently, reduced LPS-induced nuclear factor κB (NFκB) DNA binding activities, as well as the transcriptional activity of NFκB, leading to the decreased expression of NFκB-target genes, including tumor necrosis factor-α, interleukin (IL)-6, IL-1β, inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2, as well as transcriptional activity of iNOS and COX-2.These results indicate that erucin exerts a potent anti-inflammatory activity by inhibiting the pro-inflammatory enzymes and cytokines, which may be mediated, at least in part, via the inhibition of NFκB signaling.

View Article: PubMed Central - PubMed

Affiliation: Department of Food and Nutrition, Hallym University, Chuncheon 200-702, Korea. jyoon@hallym.ac.kr.

ABSTRACT
Erucin, an isothiocyanate, is a hydrolysis product of glucoerucin found in arugula and has recently been reported to have anti-cancer properties in various cancer cells. In this study, we assessed the anti-inflammatory effects of erucin and the underlying mechanisms, using lipopolysaccharide (LPS)-stimulated RAW 264.7 murine macrophages and 12-O-tetradecanoylphorbol-13-acetate-treated mouse skin. In RAW 264.7 cells, erucin (2.5, 5 μmol/L) inhibited LPS-induced production of nitric oxide and prostaglandin E2. Erucin inhibited LPS-induced degradation of the inhibitor of κBα and translocation of p65 to the nucleus and, subsequently, reduced LPS-induced nuclear factor κB (NFκB) DNA binding activities, as well as the transcriptional activity of NFκB, leading to the decreased expression of NFκB-target genes, including tumor necrosis factor-α, interleukin (IL)-6, IL-1β, inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2, as well as transcriptional activity of iNOS and COX-2. In mice, erucin (100, 300 nmoles) treatment significantly inhibited phorbol ester-induced formation of ear edema and expression of iNOS and COX-2 proteins. These results indicate that erucin exerts a potent anti-inflammatory activity by inhibiting the pro-inflammatory enzymes and cytokines, which may be mediated, at least in part, via the inhibition of NFκB signaling.

Show MeSH
Related in: MedlinePlus