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Butein, a tetrahydroxychalcone, suppresses pro-inflammatory responses in HaCaT keratinocytes.

Seo WY, Youn GS, Choi SY, Park J - BMB Rep (2015)

Bottom Line: In this study, we examined the anti-inflammatory effects of butein, a tetrahydroxychalcone, and its action mechanisms using TNF-α-stimulated keratinocytes.Butein decreased TNF-α-induced ROS generation in a dose-dependent manner in HaCaT cells.Overall, our results indicate that butein has immunomodulatory activities by inhibiting expression of pro-inflammatory mediators in keratinocytes.

View Article: PubMed Central - PubMed

Affiliation: Department of Biomedical Science and Research Institute for Bioscience & Biotechnology, Hallym University, Chuncheon 24252, Korea.

ABSTRACT
Up-regulation of cell adhesion molecules and pro-inflammatory cytokines contributes to enhanced monocyte adhesiveness and infiltration into the skin, during the pathogenesis of various inflammatory skin diseases, including atopic dermatitis. In this study, we examined the anti-inflammatory effects of butein, a tetrahydroxychalcone, and its action mechanisms using TNF-α-stimulated keratinocytes. Butein significantly inhibited TNF-α-induced ICAM-I expression and monocyte adhesion in human keratinocyte cell line HaCaT. Butein also decreased TNF-α-induced pro-inflammatory mediators, such as IL-6, IP-10 and MCP-1, in HaCaT cells. Butein decreased TNF-α-induced ROS generation in a dose-dependent manner in HaCaT cells. In addition, treatment of HaCaT cells with butein suppressed TNF-α-induced MAPK activation. Furthermore, butein suppressed TNF-α-induced NF-kappaB activation. Overall, our results indicate that butein has immunomodulatory activities by inhibiting expression of pro-inflammatory mediators in keratinocytes. Therefore, butein may be used as a therapeutic agent for the treatment of inflammatory skin diseases.

No MeSH data available.


Related in: MedlinePlus

Inhibitory effect of butein on TNF-α-induced ROS generation and MAPK activation in HaCaT cells. (A) HaCaT cells were pretreated with 2, 5 and 10 μM butein for 4 h, and then exposed to 10 ng/ml TNF-α for 15 min. Intracellular ROS levels were assessed by staining with DCF-DA using an ELISA plate reader. The results are expressed as mean ±SD of three independent experiments. Statistical significance: **P < 0.01 and ***P < 0.001 compared to TNF-α alone. (B) Cells were pretreated with 2, 5 and 10 μM butein for 4 h, and then exposed to 10 ng/ml TNF-α for 15 min. Cells extracts were prepared, and analyzed for MAPK activation by Western blot analysis, using specific antibodies. (C) Relative protein levels in the (B) panel were quantified by scanning densitometry, and normalized to control protein levels. The results are expressed as mean ±SD of three independent experiments. Statistical significance: **P < 0.01 compared to TNF-α alone.
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Figure 003: Inhibitory effect of butein on TNF-α-induced ROS generation and MAPK activation in HaCaT cells. (A) HaCaT cells were pretreated with 2, 5 and 10 μM butein for 4 h, and then exposed to 10 ng/ml TNF-α for 15 min. Intracellular ROS levels were assessed by staining with DCF-DA using an ELISA plate reader. The results are expressed as mean ±SD of three independent experiments. Statistical significance: **P < 0.01 and ***P < 0.001 compared to TNF-α alone. (B) Cells were pretreated with 2, 5 and 10 μM butein for 4 h, and then exposed to 10 ng/ml TNF-α for 15 min. Cells extracts were prepared, and analyzed for MAPK activation by Western blot analysis, using specific antibodies. (C) Relative protein levels in the (B) panel were quantified by scanning densitometry, and normalized to control protein levels. The results are expressed as mean ±SD of three independent experiments. Statistical significance: **P < 0.01 compared to TNF-α alone.

Mentions: Exposure of the keratinocytes to a variety of stimuli, such as cytokines and TPA, leads to the excessive generation of reactive oxygen species (ROS) (4) We further examined the effect of butein on TNF-α-induced ROS generation. Cells were pretreated with butein, exposed to TNF-α for 1 h and then the levels of ROS in cells were determined, using DCF-DA as a probe. As shown in Fig. 3A, butein significantly inhibited TNF--α-induced ROS production in HaCaT cells.


Butein, a tetrahydroxychalcone, suppresses pro-inflammatory responses in HaCaT keratinocytes.

Seo WY, Youn GS, Choi SY, Park J - BMB Rep (2015)

Inhibitory effect of butein on TNF-α-induced ROS generation and MAPK activation in HaCaT cells. (A) HaCaT cells were pretreated with 2, 5 and 10 μM butein for 4 h, and then exposed to 10 ng/ml TNF-α for 15 min. Intracellular ROS levels were assessed by staining with DCF-DA using an ELISA plate reader. The results are expressed as mean ±SD of three independent experiments. Statistical significance: **P < 0.01 and ***P < 0.001 compared to TNF-α alone. (B) Cells were pretreated with 2, 5 and 10 μM butein for 4 h, and then exposed to 10 ng/ml TNF-α for 15 min. Cells extracts were prepared, and analyzed for MAPK activation by Western blot analysis, using specific antibodies. (C) Relative protein levels in the (B) panel were quantified by scanning densitometry, and normalized to control protein levels. The results are expressed as mean ±SD of three independent experiments. Statistical significance: **P < 0.01 compared to TNF-α alone.
© Copyright Policy - open-access
Related In: Results  -  Collection

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Figure 003: Inhibitory effect of butein on TNF-α-induced ROS generation and MAPK activation in HaCaT cells. (A) HaCaT cells were pretreated with 2, 5 and 10 μM butein for 4 h, and then exposed to 10 ng/ml TNF-α for 15 min. Intracellular ROS levels were assessed by staining with DCF-DA using an ELISA plate reader. The results are expressed as mean ±SD of three independent experiments. Statistical significance: **P < 0.01 and ***P < 0.001 compared to TNF-α alone. (B) Cells were pretreated with 2, 5 and 10 μM butein for 4 h, and then exposed to 10 ng/ml TNF-α for 15 min. Cells extracts were prepared, and analyzed for MAPK activation by Western blot analysis, using specific antibodies. (C) Relative protein levels in the (B) panel were quantified by scanning densitometry, and normalized to control protein levels. The results are expressed as mean ±SD of three independent experiments. Statistical significance: **P < 0.01 compared to TNF-α alone.
Mentions: Exposure of the keratinocytes to a variety of stimuli, such as cytokines and TPA, leads to the excessive generation of reactive oxygen species (ROS) (4) We further examined the effect of butein on TNF-α-induced ROS generation. Cells were pretreated with butein, exposed to TNF-α for 1 h and then the levels of ROS in cells were determined, using DCF-DA as a probe. As shown in Fig. 3A, butein significantly inhibited TNF--α-induced ROS production in HaCaT cells.

Bottom Line: In this study, we examined the anti-inflammatory effects of butein, a tetrahydroxychalcone, and its action mechanisms using TNF-α-stimulated keratinocytes.Butein decreased TNF-α-induced ROS generation in a dose-dependent manner in HaCaT cells.Overall, our results indicate that butein has immunomodulatory activities by inhibiting expression of pro-inflammatory mediators in keratinocytes.

View Article: PubMed Central - PubMed

Affiliation: Department of Biomedical Science and Research Institute for Bioscience & Biotechnology, Hallym University, Chuncheon 24252, Korea.

ABSTRACT
Up-regulation of cell adhesion molecules and pro-inflammatory cytokines contributes to enhanced monocyte adhesiveness and infiltration into the skin, during the pathogenesis of various inflammatory skin diseases, including atopic dermatitis. In this study, we examined the anti-inflammatory effects of butein, a tetrahydroxychalcone, and its action mechanisms using TNF-α-stimulated keratinocytes. Butein significantly inhibited TNF-α-induced ICAM-I expression and monocyte adhesion in human keratinocyte cell line HaCaT. Butein also decreased TNF-α-induced pro-inflammatory mediators, such as IL-6, IP-10 and MCP-1, in HaCaT cells. Butein decreased TNF-α-induced ROS generation in a dose-dependent manner in HaCaT cells. In addition, treatment of HaCaT cells with butein suppressed TNF-α-induced MAPK activation. Furthermore, butein suppressed TNF-α-induced NF-kappaB activation. Overall, our results indicate that butein has immunomodulatory activities by inhibiting expression of pro-inflammatory mediators in keratinocytes. Therefore, butein may be used as a therapeutic agent for the treatment of inflammatory skin diseases.

No MeSH data available.


Related in: MedlinePlus