Background: Ginseng has been used in Korea for a long time as a restorative herbal medicine. Black ginseng (BG) is made from red or white ginseng by multiple steamy and dry processes. Although BG has been reported to have anti-inflammatory potential, studies on its influence on inflammatory skin disorders are lacking. Objective: To investigate the effects of BG under the inflammatory conditions of cultured sebocytes and outer root sheath (ORS) cells. Methods: The cultured cells were treated with 0.1% dimethyl sulfoxide, 5 μg/ml lipopolysaccharide (LPS) or 5 μg/ml LPS+50 μg/ml BG for 6 hours and 24 hours. Reverse transcription-polymerase chain reaction (RT-PCR), real-time PCR, enzyme-linked immunosorbent assay, western blotting, immunofluorescence staining and Nile red staining were performed for analysis of inflammatory biomarkers and sebum-related biomarkers. Results: BG brought out the increased gene and protein expression of inflammatory biomarkers such as interleukin (IL)-1β, IL-6, IL-8, and tumor necrosis factor-a, in the LPStreated sebocytes and ORS cells. In addition, BG induced increased expression of TLR4, p-c-jun, p-JNK and p-iκB in LPS-treated sebocytes and ORS cells. Furthermore, it significantly increased the expression of LL-37 and the production of sebum in LPS-treated sebocytes. Conclusion It may be possible for BG to increase the expression of inflammatory biomarkers in inflammatory skin disorders, such as acne.

Background: Particulate matter (PM) is an air pollutant that can impair the human skin.Antioxidants have been tested to improve PM-induced skin inflammation. Objective: In this study, we investigated the effects of dieckol on PM-induced inflammation on cultured human sebocytes, outer root sheath (ORS) cells, and mice pretreated with Cutibacterium acnes. Methods: We cultured and treated the sebocytes and ORS cells with 5 μM of dieckol and 100 μg/ml of PM10 for 24 h. The C. acnes−pretreated mice received 5 μM of dieckol and 100 μg/ml of PM10. We measured cell viability using MTT assay. Real-time PCR and measurement of reactive oxygen species (ROS) and sebum production analyzed the effects. Results: Dieckol inhibited the upregulation of the gene expression of the inflammatory cytokines, matrix metalloproteinase (MMP), aryl hydrocarbon receptor, and nuclear factor kappa-light-chain-enhancer of activated B cells by PM10 in the cultured sebocytes and ORS cells and inhibited an increase in ROS production by PM10 in the cultured sebocytes.In addition, dieckol decreased the inflammatory cytokines, MMP, and sebum production in C. acnes−pretreated mice. Conclusion Dieckol effectively reduced the expression of inflammatory biomarkers and the production of sebum in cultured sebocytes, ORS cells, and C. acnes−pretreated mice.

Background: Particulate matter (PM) is one of the air pollutants that can damage human skin; the recent increase in the amount of PM may be detrimental to skin health. Objective: We aimed to investigate the effects of PM on cultured human sebocytes and outer root sheath (ORS) cells and the effects of Siegesbeckia Herba extract (SHE) on PM-treated cultured cells. Methods: Sebocytes and ORS cells were cultured. The cultured cells were treated with various concentrations of PM of <10 μm in size (PM10) (10 μg/ml, 25 μg/ml, 50 μg/ml, and 100 μg/ml) for 24 h. Real-time polymerase chain reaction, measurement of reactive oxygen species (ROS), small interfering (si) RNA transfection, Oil Red O and Nile red staining, and immunofluorescence staining were performed to analyze the presence of inflammatory cytokines, matrix metalloproteinases (MMPs), aryl hydrocarbon receptor (AhR), nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB), ROS, and lipid production. In addition, PM10 (100 μg/ml)-treated cultured cells were treated with 10 mg/ml of SHE. Results: PM10 upregulates the expression of inflammatory cytokines, MMPs, AhR, NFkB, and ROS in cultured human sebocytes and ORS cells. The production of ROS was dramatically reduced in AhR siRNA-transfected cells. In addition, PM10 upregulates sebum production in cultured sebocytes. SHE inhibited the upregulation of inflammatory cytokines, MMPs, AhR, NF-kB, ROS, and sebum production in cultured human sebocytes and/or ORS cells by PM10. Conclusion Effects of PM10 on cultured human sebocytes and ORS cells can be regulated by SH.

Background: Ginseng has been known in Korea as a healthsupportive herbal medicine from time immemorial. Essential oil isolated from fresh ginseng has been shown to display antibacterial and anti-inflammatory activities. Objective: The effects of red ginseng oil (RGO) on the lipopolysaccharide (LPS)-treated sebocytes and outer root sheath (ORS) cells were studied. Methods: The cultured cells were treated with either 0.1% dimethyl sulfoxide, 5 μg/ml LPS, 50 μg/ml RGO, or 5 μg/ml LPS plus 50 μg/ml RGO for 6 and 24 hours.RT-PCR, real-time PCR, enzyme-linked immunosorbent assay, western blot, and immunofluorescence staining were performed for the analysis of inflammatory cytokine. Results: RGO showed the increased gene and protein expression of inflammatory cytokines, including interleukin (IL)-1β, IL-6, IL-8, and tumor necrosis factor-α in the LPS-treated sebocytes and ORS cells. RGO also showed the increased protein expression of p-c-jun and p-JNK in the LPS-treated sebocytes and ORS cells. Gene expression of TLR2 was increased in LPS-treated sebocytes following treatment with RGO. Additionally, RGO resulted in an increased expression of LL-37 in the LPS-treated sebocytes and ORS cells. Moreover, it remarkably increased the production of sebum in LPS-treated sebocytes. Conclusion RGO might be among the aggravating factors of acne vulgaris. It would be better to stop taking red ginseng in patients with inflammatory acne.

Background: Although ginseng has beneficial effects largely related to their constituent ginsenosides, pharmacological effects of non-ginsenosides have been reported. Acidic polysaccharides of red ginseng (RGAP) are among the non-ginsenoside constituents that have characterized antioxidant properties. Objective: We investigated the impact of RGAP on sebocytes and outer root sheath (ORS) cells treated with lipopolysaccharide (LPS) and in mice with Cutibacterium acnes (C. acnes)-induced inflammatory nodules. Methods: Sebocytes and ORS cells were cultured and treated with either 0.1% dimethyl sulfoxide, 5 μg/ml LPS, 50 μg/ml RGAP or 5 μg/ml LPS+50 μg/ml RGAP for 6 and 24 hours.Real-time polymerase chain reaction, ELISA, Western blot analysis, and immunofluorescence staining were among the methods used to detect and quantify inflammatory cytokine production. Mice infected with C. acnes were treated with 2 weeks of RGAP provided in drinking water followed by immunohistochemical evaluation of inflammatory nodules. Results: Administration of RGAP to LPS-treated sebocytes and ORS cell cultures resulted in increased expression of inflammatory cytokines like interleukin (IL)-1β, IL-6, IL-8, and tumor necrosis factor-α, toll-like receptor 2, p-c-jun, p-JNK and p-iKB (p＜0.05). Administration of RGAP also resulted in increased expression of LL37 in LPS-treated sebocytes and ORS cells, and increased production of sebum in LPS-treated sebocytes (p＜0.05). RGAP also promoted increased expression of inflammatory biomarkers in C. acnes-associated inflammatory nodules in mice (p＜0.05). Conclusion RGAP may exacerbate inflammatory pathology associated with acne vulgaris. Ginseng supplements may be contraindicated in patients diagnosed with inflammatory acne.

Background: Ginseng has been known in Korea as a healthsupportive herbal medicine from time immemorial. Essential oil isolated from fresh ginseng has been shown to display antibacterial and anti-inflammatory activities. Objective: The effects of red ginseng oil (RGO) on the lipopolysaccharide (LPS)-treated sebocytes and outer root sheath (ORS) cells were studied. Methods: The cultured cells were treated with either 0.1% dimethyl sulfoxide, 5 μg/ml LPS, 50 μg/ml RGO, or 5 μg/ml LPS plus 50 μg/ml RGO for 6 and 24 hours.RT-PCR, real-time PCR, enzyme-linked immunosorbent assay, western blot, and immunofluorescence staining were performed for the analysis of inflammatory cytokine. Results: RGO showed the increased gene and protein expression of inflammatory cytokines, including interleukin (IL)-1β, IL-6, IL-8, and tumor necrosis factor-α in the LPS-treated sebocytes and ORS cells. RGO also showed the increased protein expression of p-c-jun and p-JNK in the LPS-treated sebocytes and ORS cells. Gene expression of TLR2 was increased in LPS-treated sebocytes following treatment with RGO. Additionally, RGO resulted in an increased expression of LL-37 in the LPS-treated sebocytes and ORS cells. Moreover, it remarkably increased the production of sebum in LPS-treated sebocytes. Conclusion RGO might be among the aggravating factors of acne vulgaris. It would be better to stop taking red ginseng in patients with inflammatory acne.

Background: Although ginseng has beneficial effects largely related to their constituent ginsenosides, pharmacological effects of non-ginsenosides have been reported. Acidic polysaccharides of red ginseng (RGAP) are among the non-ginsenoside constituents that have characterized antioxidant properties. Objective: We investigated the impact of RGAP on sebocytes and outer root sheath (ORS) cells treated with lipopolysaccharide (LPS) and in mice with Cutibacterium acnes (C. acnes)-induced inflammatory nodules. Methods: Sebocytes and ORS cells were cultured and treated with either 0.1% dimethyl sulfoxide, 5 μg/ml LPS, 50 μg/ml RGAP or 5 μg/ml LPS+50 μg/ml RGAP for 6 and 24 hours.Real-time polymerase chain reaction, ELISA, Western blot analysis, and immunofluorescence staining were among the methods used to detect and quantify inflammatory cytokine production. Mice infected with C. acnes were treated with 2 weeks of RGAP provided in drinking water followed by immunohistochemical evaluation of inflammatory nodules. Results: Administration of RGAP to LPS-treated sebocytes and ORS cell cultures resulted in increased expression of inflammatory cytokines like interleukin (IL)-1β, IL-6, IL-8, and tumor necrosis factor-α, toll-like receptor 2, p-c-jun, p-JNK and p-iKB (p＜0.05). Administration of RGAP also resulted in increased expression of LL37 in LPS-treated sebocytes and ORS cells, and increased production of sebum in LPS-treated sebocytes (p＜0.05). RGAP also promoted increased expression of inflammatory biomarkers in C. acnes-associated inflammatory nodules in mice (p＜0.05). Conclusion RGAP may exacerbate inflammatory pathology associated with acne vulgaris. Ginseng supplements may be contraindicated in patients diagnosed with inflammatory acne.

Background: Particulate matters (PM) comprise a heterogeneous mixture of particles suspended in air. A recent study found that urban PMs may penetrate into hair follicles via transfollicular and transdermal routes in dorsal skin. Objective: To investigate the effects of PM on ex vivo cultured human scalp hair follicles and hair follicular keratinocytes in vitro. Methods: TUNEL staining was employed to check cells undergoing apoptosis in cultured hair follicles after PM treatment. MTT assay was employed to check cell viability after PM treatment. Quantitative real-time PCR analysis was employed to quantitate the expression of inflammatory genes, matrix metalloproteinases (MMPs), and Duox1. Inflammatory cytokine levels were measured by ELISA after PM treatment. The level of reactive oxygen species (ROS) production was measured using a chemical fluorescent probe by a fluorescence plate reader. Results: Abundant TUNEL-positive cells were observed in the keratinocyte region of hair including the epidermis, sebaceous gland, outer root sheath (ORS), inner root sheath (IRS), and bulb region. The viability of follicular cells, including the ORS, was found to be decreased upon PM exposure. mRNA expression and protein levels of inflammatory response genes and MMPs were upregulated in a dose-dependent manner by PM treatment. ROS levels were also increased by PM. Conclusion These data strongly suggest that penetrated PMs from air pollution may cause apoptotic cell death to follicular keratinocytes by increased production of ROS and inflammatory cytokines, which could impair hair growth.