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Anti-inflammatory potential of allyl-isothiocyanate--role of Nrf2, NF-(κ) B and microRNA-155.

Wagner AE, Boesch-Saadatmandi C, Dose J, Schultheiss G, Rimbach G - J. Cell. Mol. Med. (2012)

Bottom Line: AITC decreased nuclear p65 protein levels, a subunit of the transcription factor NF-κB.Importantly, our data indicate that AITC significantly attenuated microRNA-155 levels in LPS-stimulated RAW264.7 macrophages in a dose-dependent manner.The anti-inflammatory effects of AITC were accompanied by an increase in Nrf2 nuclear translocation and consequently by an increase of mRNA and protein levels of the Nrf2 target gene heme-oxygenase 1.

View Article: PubMed Central - PubMed

Affiliation: Institute of Human Nutrition and Food Science, Christian-Albrechts-University, Kiel, Germany. wagner@molecularnutrition.uni-kiel.de

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Related in: MedlinePlus

Effect of allyl-isothiocyanate (AITC) on IL-1β, iNOS and miR-155 in mice fed a pro-inflammatory high-fat diet. Female C57BL/6 mice were fed a pro-inflammatory high-fat diet for eight weeks. After seven weeks, the mice were applied 15 mg AITC per kg body weight or PBS (control) via oral gavage daily for seven days. Following RNA extraction from mouse liver levels of IL-1β (A), iNOS (B) and miR-155 (C) were measured by real-time PCR. Each bar represents the mean (±S.E.M.) from nine or 10 animals. Means without a common letter differ significantly (P < 0.05).
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fig08: Effect of allyl-isothiocyanate (AITC) on IL-1β, iNOS and miR-155 in mice fed a pro-inflammatory high-fat diet. Female C57BL/6 mice were fed a pro-inflammatory high-fat diet for eight weeks. After seven weeks, the mice were applied 15 mg AITC per kg body weight or PBS (control) via oral gavage daily for seven days. Following RNA extraction from mouse liver levels of IL-1β (A), iNOS (B) and miR-155 (C) were measured by real-time PCR. Each bar represents the mean (±S.E.M.) from nine or 10 animals. Means without a common letter differ significantly (P < 0.05).

Mentions: No significant changes in feed intake (1.89 ± 0.46 versus 1.61 ± 0.57 g/d) and body weight gain (2.04 ± 0.57 versus 1.87 ± 0.48 g) between control and AITC-treated mice were observed during the study period. A 7-day-oral-application of AITC in mice fed a high-fat diet resulted in an increase in nuclear Nrf2 protein levels in the liver (Fig. 7C). This increase in nuclear Nrf2 protein was accompanied by a significant increase in Nrf2 and HO-1 mRNA levels (Fig. 7A and B). Administration of AITC resulted also in a moderate but not significant down-regulation of IL-1β, iNOS and miR-155 levels (Fig. 8A–C) in mouse liver. TNF-α mRNA levels were not affected by AITC treatment (data not shown). In an independent experiment, mice were fed either a low-fat standard or a high-fat diet for 8 weeks resulting in an increase of IL-1β liver mRNA levels in the high-fat diet as compared to the low-fat standard diet group. This observation is in line with literature data [24, 25], indicating an induction of pro-inflammatory markers in mice consuming a high-fat diet.


Anti-inflammatory potential of allyl-isothiocyanate--role of Nrf2, NF-(κ) B and microRNA-155.

Wagner AE, Boesch-Saadatmandi C, Dose J, Schultheiss G, Rimbach G - J. Cell. Mol. Med. (2012)

Effect of allyl-isothiocyanate (AITC) on IL-1β, iNOS and miR-155 in mice fed a pro-inflammatory high-fat diet. Female C57BL/6 mice were fed a pro-inflammatory high-fat diet for eight weeks. After seven weeks, the mice were applied 15 mg AITC per kg body weight or PBS (control) via oral gavage daily for seven days. Following RNA extraction from mouse liver levels of IL-1β (A), iNOS (B) and miR-155 (C) were measured by real-time PCR. Each bar represents the mean (±S.E.M.) from nine or 10 animals. Means without a common letter differ significantly (P < 0.05).
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3822852&req=5

fig08: Effect of allyl-isothiocyanate (AITC) on IL-1β, iNOS and miR-155 in mice fed a pro-inflammatory high-fat diet. Female C57BL/6 mice were fed a pro-inflammatory high-fat diet for eight weeks. After seven weeks, the mice were applied 15 mg AITC per kg body weight or PBS (control) via oral gavage daily for seven days. Following RNA extraction from mouse liver levels of IL-1β (A), iNOS (B) and miR-155 (C) were measured by real-time PCR. Each bar represents the mean (±S.E.M.) from nine or 10 animals. Means without a common letter differ significantly (P < 0.05).
Mentions: No significant changes in feed intake (1.89 ± 0.46 versus 1.61 ± 0.57 g/d) and body weight gain (2.04 ± 0.57 versus 1.87 ± 0.48 g) between control and AITC-treated mice were observed during the study period. A 7-day-oral-application of AITC in mice fed a high-fat diet resulted in an increase in nuclear Nrf2 protein levels in the liver (Fig. 7C). This increase in nuclear Nrf2 protein was accompanied by a significant increase in Nrf2 and HO-1 mRNA levels (Fig. 7A and B). Administration of AITC resulted also in a moderate but not significant down-regulation of IL-1β, iNOS and miR-155 levels (Fig. 8A–C) in mouse liver. TNF-α mRNA levels were not affected by AITC treatment (data not shown). In an independent experiment, mice were fed either a low-fat standard or a high-fat diet for 8 weeks resulting in an increase of IL-1β liver mRNA levels in the high-fat diet as compared to the low-fat standard diet group. This observation is in line with literature data [24, 25], indicating an induction of pro-inflammatory markers in mice consuming a high-fat diet.

Bottom Line: AITC decreased nuclear p65 protein levels, a subunit of the transcription factor NF-κB.Importantly, our data indicate that AITC significantly attenuated microRNA-155 levels in LPS-stimulated RAW264.7 macrophages in a dose-dependent manner.The anti-inflammatory effects of AITC were accompanied by an increase in Nrf2 nuclear translocation and consequently by an increase of mRNA and protein levels of the Nrf2 target gene heme-oxygenase 1.

View Article: PubMed Central - PubMed

Affiliation: Institute of Human Nutrition and Food Science, Christian-Albrechts-University, Kiel, Germany. wagner@molecularnutrition.uni-kiel.de

Show MeSH
Related in: MedlinePlus