RESUMO
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.
RESUMO
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.
RESUMO
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.
RESUMO
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.
RESUMO
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.
RESUMO
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.
RESUMO
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.
RESUMO
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.
RESUMO
Fatty acid-CoA ligase 4 (FACL4) is a central enzyme controlling the unesterified free arachidonic acid (AA) level in cells and the free AA is known to induce apoptosis. We have recently reported that expression of FACL4 is upregulated in about 40% of human hepatocellular carcinoma (HCC) and 50% of HCC cell lines, suggesting that FACL4 may be involved in liver carcinogenesis. In this study, we investigated whether HCC cell growth is regulated by FACL4. Immunoblot analysis showed that SNU 398 cells express very low or no detectable level of FACL4. We, therefore, transfected the SNU 398 cells with FACL4 expression vector, and clones expressing FACL4 were pooled and analyzed. We found that forced expression of FACL4 in SNU 398 promotes the growth of cells. In addition, we observed that triacsin C, a FACL4 inhibitor, inhibits the growth of Hep 3B cell line which expresses high level of endogenous FACL4. We also found that the triacsin C-mediated growth inhibition in Hep 3B cells results from the induction of apoptosis with evidence of Bcl-2 reduction. Altogether, our data show that FACL4 affects HCC cell growth and suggest that modulation of FACL4 expression/activity is an approach for treatment of HCC.
Assuntos
Humanos , Apoptose , Carcinoma Hepatocelular/enzimologia , Linhagem Celular Tumoral , Proliferação de Células , Coenzima A Ligases/antagonistas & inibidores , Neoplasias Hepáticas/enzimologia , Proteínas Proto-Oncogênicas c-bcl-2/metabolismo , Triazenos/farmacologiaRESUMO
PURPOSE: Recent studies have shown that Dickkopf-1 (DKK-1) is overexpressed in some tumors, including hepatocellular carcinoma. However, the role of increased DKK-1 in these tumors is not known. In this study, the DKK-1 expression in hepatocellular carcinoma (HCC) cell lines was evaluated and the effect of DKK-1 overexpression in HCC cell lines was studied. MATERIALS AND METHODS: The expression of DKK-1 in hepatocellular carcinoma cell lines was evaluated by RT-PCR. Stable cell lines that overexpressed DKK-1 were established. Cell growth, adhesion, migration and invasion assays were performed. RESULTS: RT-PCR analysis showed that 5 out of 8 HCC cell lines expressed DKK-1. The forced expression of DKK-1 suppressed the growth of cells and increased the population of cells in the sub-G1 phase. In addition, DKK- 1 reduced the cellular adhesion capacity to collagen type I and fibronectin, and it increased migratory capacity. However, overexpression of DKK-1 did not increase the invasion capacity of the HCC cell line. CONCLUSION: Collectively, our data suggest that overexpression of DKK-1 affects the biology of HCC cells.