• Journal of Physiology & Pathology in Korean Medicine
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• v.28 no.2
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• pp.146-153
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• 2014

Gami-Sopungsan (GS) is one of the traditional korean remedy. We investigated the anti-inflammation and anti-atopic dermatitis (AD) effect of GS. No cytotoxicity of GS was observed in the range of $1{\sim}100{\mu}g/m{\ell}$ on Raw 264.7 cells. The Inflammatory response of Raw 264.7 cells were induced by lipopolysaccharide (LPS), followed by GS treatment at indicated concentrations (0, 1, 10 and $100{\mu}g/m{\ell}$). At $100{\mu}g/m{\ell}$ concentration, GS showed inhibitory effect on LPS-induced nitric oxide production by 20%. Production of IL-$1{\beta}$, IL-6 and TNF-${\alpha}$ was decreased by approximately 56%, 36% and 79%, respectively upon GS treatment at $100{\mu}g/m{\ell}$. 200 mg/kg of GS was orally administered to NC/Nga mice, where AD was induced by 1-chloro 2,4-dinitrobenzene. There were no significant difference between GS treated group and the control group on body weight and food intake changes during growth. The back skin of GS group showed decrease in erythema, pruritus, dry skin, edema, excoriation, erosion and lichenification level through naked eye observations. In addition, leukocyte infiltration and the thickness of epidermis were significantly decreased in the skin tissues (back and ear). The serum IgE levels were decreased by 28.8% in the GS treated group. The GS treated group showed remarkable inhibition of IL-4 (83%), IL-5 (95%), IL-6 (62%) and TNF-${\alpha}$ (84%) in serum, indicating that GS has similar or higher efficacy than those of the dexamethasone treated group. From the results above, we conclude that GS has significant anti-inflammation and anti-AD effects on Raw 264.7 cells and NC/Nga mice. The results should provide fundamental and valuable data for the research on natural products being developed against atopic dermatitis.

• Korean Journal of Clinical Laboratory Science
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• v.49 no.2
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• pp.150-160
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• 2017

Atopic dermatitis (AD) is a chronic inflammatory skin disease. It is characterized by eczematous lesions, skin dryness, and pruritus. The existing treatment drugs for AD have side effects, especially if the drugs are taken for extended periods. Therefore, new alternative therapies are necessary. The aim of this study was to investigate the combined effects of curcumin administration and LED irradiation on AD. AD-like lesions were induced in BALB/c mice by repeated application of 1-chloro-2,4-dinitrobenzene (DNCB) to the shaved skin of the ear and neck. Thirty male BALB/c mice were divided into five groups: vehicle, DNCB, curcumin, LED, and curcumin+LED groups. Curcumin (0.1 g/kg/day) was administrated repeatedly during a period of 14 days (experimental period) and 630 nm LED irradiation ($5J/cm^2/day$) was performed in the acryl box once a day for 10 days, after inducing AD-like lesions via DNCB application. The severity of AD-like lesions was evaluated during the experimental period, using a modified SCORAD index. Both ear and neck skin tissues were examined histologically for epidermal thickness, mast cell, eosinophil counting, and dermal collagen density. Epidermal cell proliferation and apoptosis were detected using immunohistochemistry and TUNEL, respectively. These were all reduced in SCORAD index, epidermal thickness, collagen density, number of mast cell and eosinophil in dermis, and number of proliferating cell and apoptotic cell in epidermis by curcumin administration and 630 nm LED irradiation. Moreover, all parameters were significantly lower in the curcumin+LED group compared with the curcumin group and LED group. These results suggest that the combined therapy of curcumin and LED is more effective than a single treatment. We recommend that this can be a feasible alternative therapy to manage AD.

• Journal of Ginseng Research
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• v.44 no.6
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• pp.799-807
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• 2020

Background: The skin acts as a barrier to protect organisms against harmful exogenous agents. Compound K (CK) is an active metabolite of ginsenoside Rb1, Rb2 and Rc, and researchers have focused on its skin protective efficacy. In this study, we hypothesized that increased expression of the serine protease inhibitor Kazal type-5 (SPINK5) may improve skin barrier function. Methods: We screened several ginsenosides to increase SPINK5 gene promoter activity using a transactivation assay and found that CK can increase SPINK5 expression. To investigate the protective effect of CK on the skin barrier, RT-PCR and Western blotting were performed to investigate the expression levels of SPINK5, kallikrein 5 (KLK5), KLK7 and PAR2 in UVB-irradiated HaCaT cells. Measurement of transepidermal water loss (TEWL) and histological changes associated with the skin barrier were performed in a UVB-irradiated mouse model and a 1-chloro-2,4-dinitrobenzene (DNCB)-induced atopic dermatitis-like model. Results: CK treatment increased the expression of SPINK5 and decreased the expression of its downstream genes, such as KLKs and PAR2. In the UVB-irradiated mouse model and the DNCB-induced atopic dermatitis model, CK restored increased TEWL and decreased hydration and epidermal hyperplasia. In addition, CK normalized the reduced SPINK5 expression caused by UVB or DNCB, thereby restoring the expression of the proteins involved in desquamation to a level similar to normal. Conclusions: Our data showed that CK contributes to improving skin-barrier function in UVB-irradiated and DNCB-induced atopic dermatitis-like models through SPINK5. These results suggest that therapeutic attempts with CK might be useful in treating barrier-disrupted diseases.

• Korean Journal of Environmental Agriculture
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• v.14 no.3
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• pp.329-337
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• 1995

The effect of N-(4-chlorophenyl) maleimide(CPMI), plant growth regulators, and alkylating agents on gluathione(GSH) content and glutathione S-transferase(GST) activity was examined with 3-day-old etiolated sorghum(Sorghum bicolor [L.] Moench) seedlings. The GSH content and GST activity of untreated seedlings were higher in shoots than that in roots. Response of GST activity in coleoptile was significantly greater than in other tissues of sorghum seedling. In CPMI-treated seedlings, GSH content was not significantly different from that in untreated seedlings. CPM treatment resulted in 2.3-fold increase in GST activity measured with metolachlor as substrate in the coleoptile region. In contrast, change in GST activity measured with metolachlor as substrate in the coleoptile region. In contrast, change in GST activity measured with 1-chloro-2, 4-dinitrobenzene did not occur. The increase of GST activity was caused by induction of a GST isozyme, which is substrate-specific to metolachlor. Subsequently, two hypotheses related to metolachlor detoxification were evaluated on the basis of regulation of plant growth regulators and substrate induction of GST activity. In coleoptile, GST activity measured with metolachior was increased to 2.1-and 3.4-fold by both 2, 4-dichlorophenoxyacetic acid(2,4-D) and metolachlor treated at the germination stage of sorghum, respectively. Treatments of 2.4-D and metolachlor also induced isozymes exhibiting the activity toward metolachlor. One of the isozymes was co-eluted with that induced by CPMI. These results indicated that increase in GST activity by CPMI may be partially related to auxin regulation and substrate induction.