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1.
J Invest Dermatol ; 132(12): 2700-8, 2012 Dec.
Article En | MEDLINE | ID: mdl-22763784

Acne vulgaris is the most common disease of the pilosebaceous unit. The pathogenesis of this inflammatory disease is complex, involving increased sebum production and perifollicular inflammation. To identify effective agents for factors that induce acne vulgaris, we explored the pharmacological potential of epigallocatechin-3-gallate (EGCG), which has been widely investigated as an anti-proliferative and anti-inflammatory agent. In this study, we demonstrated that topical application of EGCG to rabbit auricles reduced the size of the sebaceous glands. When applied to cultured human SZ95 sebocytes, EGCG strongly suppressed cell proliferation and lipogenesis. These actions of EGCG were reproduced in IGF-I-differentiated SZ95 sebocytes. To investigate the anti-inflammatory potential of EGCG, we evaluated pro-inflammatory cytokine synthesis in IGF-I-differentiated SZ95 sebocytes and found that expression of IL-1, IL-6, and IL-8 was decreased. These results provide early evidence that EGCG is an effective candidate for acne therapy whose mechanisms of action in IGF-I-differentiated SZ95 sebocytes include the inhibition of lipogenesis and inflammation.


Acne Vulgaris/drug therapy , Catechin/analogs & derivatives , Insulin-Like Growth Factor I/pharmacology , Lipogenesis/drug effects , Sebaceous Glands/cytology , Acne Vulgaris/immunology , Acne Vulgaris/pathology , Administration, Topical , Animals , Anti-Inflammatory Agents/pharmacology , Apoptosis/drug effects , Apoptosis/immunology , Catechin/pharmacology , Cell Line, Transformed , Cell Proliferation/drug effects , Cytokines/immunology , Cytokines/metabolism , Ear Auricle/cytology , Ear Auricle/drug effects , Female , Humans , Interleukin-1/immunology , Interleukin-1/metabolism , Interleukin-6/immunology , Interleukin-6/metabolism , Interleukin-8/immunology , Interleukin-8/metabolism , Lipogenesis/immunology , Rabbits , Sebaceous Glands/immunology , Sebaceous Glands/metabolism , Sebum/immunology , Sebum/metabolism , Signal Transduction/drug effects , Signal Transduction/immunology
2.
J Dermatol ; 39(8): 677-81, 2012 Aug.
Article En | MEDLINE | ID: mdl-22548403

As many new cosmetic products are introduced into the market, attention must be given to contact dermatitis, which is commonly caused by cosmetics. We investigate the prevalence of preservative allergy in 584 patients with suspected cosmetic contact dermatitis at 11 different hospitals. From January 2010 to March 2011, 584 patients at 11 hospital dermatology departments presented with cosmetic contact dermatitis symptoms. These patients were patch-tested for preservative allergens. An irritancy patch test performed on 30 control subjects using allergens of various concentrations showed high irritancy rates. Preservative hypersensitivity was detected in 41.1% of patients. Allergens with the highest positive test rates were benzalkonium chloride (12.1%), thimerosal (9.9%) and methylchloroisothiazolinone/methylisothiazolinone (MCI/MI) (5.5%). Benzalkonium chloride and chlorphenesin had the highest irritancy rate based on an irritancy patch test performed using various concentrations. Seven of 30 normal subjects had a positive irritant patch reading with 0.1% benzalkonium chloride and eight of 30 normal subjects had a positive irritant patch reading at 4 days with 0.5% chlorphenesin in petrolatum. Although benzalkonium chloride was highly positive for skin reactions in our study, most reactions were probably irritation. MCI/MI and thimerosal showed highly positive allergy reactions in our study. The optimum concentration of chlorphenesin to avoid skin reactions is less than 0.5%.


Cosmetics/adverse effects , Dermatitis, Allergic Contact/diagnosis , Dermatitis, Allergic Contact/epidemiology , Preservatives, Pharmaceutical/adverse effects , Adolescent , Adult , Aged , Aged, 80 and over , Benzalkonium Compounds/adverse effects , Chlorphenesin/adverse effects , Female , Humans , Male , Middle Aged , Patch Tests/statistics & numerical data , Republic of Korea/epidemiology , Thiazoles/adverse effects , Young Adult
3.
J Cutan Pathol ; 38(8): 657-62, 2011 Aug.
Article En | MEDLINE | ID: mdl-21518380

BACKGROUND: Although skin carcinogenesis has been widely investigated, only limited information is available for epidermal tumors, while even less is known about other skin structures. Alterations in the ß-catenin pathway have been reported in several epidermal tumors, while little is known about in adnexal tumors. This study was performed to assess alterations in the ß-catenin pathway associated with adnexal tumors, and to investigate the mechanisms underlying these alterations. METHODS: ß-Catenin expression in 48 adnexal tumors (trichoepithelioma, trichofolliculoma, pilomatricoma, syringoma, eccrine poroma, spiradenoma, sebaceous hyperplasia and nevus sebaceus) was assessed using immunohistochemistry. The tumors showing intense nuclear reactivity for ß-catenin were further evaluated by immunohistochemistry for ß-catenin degradation complex such as adenomatosis polyposis coli (APC), Axin and glycogen synthase kinase 3ß (GSK-3ß). RESULTS: Intense nuclear immunoreactivity for ß-catenin was observed in pilomatricoma and spiradenoma. Among 12 eccrine spiradenomas, APC was downregulated in 2 (16.7%) cases, and Axin and GSK-3ß were downregulated in 11 (91.7%) and 10 (83.3%) cases, respectively. CONCLUSIONS: This is the first reported analysis of the role of alterations in the ß-catenin pathway in spiradenoma. We suggest that downregulation of Axin and GSK-3ß in the ß-catenin pathway may be an important signaling alteration in the development of spiradenoma.


Adenoma, Sweat Gland/metabolism , Sweat Gland Neoplasms/metabolism , beta Catenin/metabolism , Adaptor Proteins, Signal Transducing/metabolism , Adenoma, Sweat Gland/pathology , Adenomatous Polyposis Coli Protein/metabolism , Axin Protein , Biomarkers, Tumor/metabolism , Cell Nucleus/metabolism , Cell Nucleus/pathology , Down-Regulation , Glycogen Synthase Kinase 3/metabolism , Glycogen Synthase Kinase 3 beta , Humans , Repressor Proteins/metabolism , Signal Transduction , Sweat Gland Neoplasms/pathology
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