Prolonged skin inflammation is caused by disrupted skin barrier resulting in chronic inflammatory diseases such as atopic dermatitis. As a potent natural product with anti-inflammatory property, Aster glehni (A. glehni) is a traditional edible herb and has been used to treat diabetes or colitis-associated colon cancer. In present study, we figured out an additional effect of A. glehni ethanol extract (AGE) in pro-inflammatory cytokines-stimulated human keratinocytes. Mixture of tumor necrosis factor-alpha (TNF-α) and interferongamma (IFN-γ) was used to induce inflammatory responses in the HaCaT keratinocytes. AGE suppressed activation of ERK mitogen-activated protein kinase, nuclear factor (NF)-κB, and signal transducer and activator of transcription 1 and 3 (STAT1 and STAT3). The treatment of AGE inhibited mRNA expressions of proinflammatory cytokines in TNF-α and IFN-γ-stimulated HaCaT cells. Also, AGE induced up-regulated expressions of skin barrier molecules like filaggrin, loricrin, or ZO-1. We evaluated the effects of AGE on protein or mRNA expression levels using western blot or qRT-PCR, respectively. Taken together, these results suggest that the treatment of AGE exerts anti-inflammatory effect on keratinocytes through suppressing inflammatory signaling pathways and up-regulating skin molecules in HaCaT keratinocytes.

Prolonged skin inflammation is caused by disrupted skin barrier resulting in chronic inflammatory diseases such as atopic dermatitis. As a potent natural product with anti-inflammatory property, Aster glehni (A. glehni) is a traditional edible herb and has been used to treat diabetes or colitis-associated colon cancer. In present study, we figured out an additional effect of A. glehni ethanol extract (AGE) in pro-inflammatory cytokines-stimulated human keratinocytes. Mixture of tumor necrosis factor-alpha (TNF-α) and interferongamma (IFN-γ) was used to induce inflammatory responses in the HaCaT keratinocytes. AGE suppressed activation of ERK mitogen-activated protein kinase, nuclear factor (NF)-κB, and signal transducer and activator of transcription 1 and 3 (STAT1 and STAT3). The treatment of AGE inhibited mRNA expressions of proinflammatory cytokines in TNF-α and IFN-γ-stimulated HaCaT cells. Also, AGE induced up-regulated expressions of skin barrier molecules like filaggrin, loricrin, or ZO-1. We evaluated the effects of AGE on protein or mRNA expression levels using western blot or qRT-PCR, respectively. Taken together, these results suggest that the treatment of AGE exerts anti-inflammatory effect on keratinocytes through suppressing inflammatory signaling pathways and up-regulating skin molecules in HaCaT keratinocytes.

Prolonged skin inflammation is caused by disrupted skin barrier resulting in chronic inflammatory diseases such as atopic dermatitis. As a potent natural product with anti-inflammatory property, Aster glehni (A. glehni) is a traditional edible herb and has been used to treat diabetes or colitis-associated colon cancer. In present study, we figured out an additional effect of A. glehni ethanol extract (AGE) in pro-inflammatory cytokines-stimulated human keratinocytes. Mixture of tumor necrosis factor-alpha (TNF-α) and interferongamma (IFN-γ) was used to induce inflammatory responses in the HaCaT keratinocytes. AGE suppressed activation of ERK mitogen-activated protein kinase, nuclear factor (NF)-κB, and signal transducer and activator of transcription 1 and 3 (STAT1 and STAT3). The treatment of AGE inhibited mRNA expressions of proinflammatory cytokines in TNF-α and IFN-γ-stimulated HaCaT cells. Also, AGE induced up-regulated expressions of skin barrier molecules like filaggrin, loricrin, or ZO-1. We evaluated the effects of AGE on protein or mRNA expression levels using western blot or qRT-PCR, respectively. Taken together, these results suggest that the treatment of AGE exerts anti-inflammatory effect on keratinocytes through suppressing inflammatory signaling pathways and up-regulating skin molecules in HaCaT keratinocytes.

Prolonged skin inflammation is caused by disrupted skin barrier resulting in chronic inflammatory diseases such as atopic dermatitis. As a potent natural product with anti-inflammatory property, Aster glehni (A. glehni) is a traditional edible herb and has been used to treat diabetes or colitis-associated colon cancer. In present study, we figured out an additional effect of A. glehni ethanol extract (AGE) in pro-inflammatory cytokines-stimulated human keratinocytes. Mixture of tumor necrosis factor-alpha (TNF-α) and interferongamma (IFN-γ) was used to induce inflammatory responses in the HaCaT keratinocytes. AGE suppressed activation of ERK mitogen-activated protein kinase, nuclear factor (NF)-κB, and signal transducer and activator of transcription 1 and 3 (STAT1 and STAT3). The treatment of AGE inhibited mRNA expressions of proinflammatory cytokines in TNF-α and IFN-γ-stimulated HaCaT cells. Also, AGE induced up-regulated expressions of skin barrier molecules like filaggrin, loricrin, or ZO-1. We evaluated the effects of AGE on protein or mRNA expression levels using western blot or qRT-PCR, respectively. Taken together, these results suggest that the treatment of AGE exerts anti-inflammatory effect on keratinocytes through suppressing inflammatory signaling pathways and up-regulating skin molecules in HaCaT keratinocytes.

Prolonged skin inflammation is caused by disrupted skin barrier resulting in chronic inflammatory diseases such as atopic dermatitis. As a potent natural product with anti-inflammatory property, Aster glehni (A. glehni) is a traditional edible herb and has been used to treat diabetes or colitis-associated colon cancer. In present study, we figured out an additional effect of A. glehni ethanol extract (AGE) in pro-inflammatory cytokines-stimulated human keratinocytes. Mixture of tumor necrosis factor-alpha (TNF-α) and interferongamma (IFN-γ) was used to induce inflammatory responses in the HaCaT keratinocytes. AGE suppressed activation of ERK mitogen-activated protein kinase, nuclear factor (NF)-κB, and signal transducer and activator of transcription 1 and 3 (STAT1 and STAT3). The treatment of AGE inhibited mRNA expressions of proinflammatory cytokines in TNF-α and IFN-γ-stimulated HaCaT cells. Also, AGE induced up-regulated expressions of skin barrier molecules like filaggrin, loricrin, or ZO-1. We evaluated the effects of AGE on protein or mRNA expression levels using western blot or qRT-PCR, respectively. Taken together, these results suggest that the treatment of AGE exerts anti-inflammatory effect on keratinocytes through suppressing inflammatory signaling pathways and up-regulating skin molecules in HaCaT keratinocytes.