• Journal of the Society of Cosmetic Scientists of Korea
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• v.41 no.4
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• pp.341-350
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• 2015

Skin carrys out protective role against harmful outer environment assaults including ultraviolet radiation, heavy metals and oxides. Especially, ultraviolet-B (UVB) light causes inflammatory reactions in skin such as sun burn and erythma and stimulates melanin pigmentation. Furthermore, the influx of UVB into skin cells causes DNA damage in keratinocytes and dermal fibroblasts, inhibition of extracellular matrix (ECM) synthesis which leads to a decrease in elasticity of skin and wrinkle formation. It also damages dermal connective tissue and disrupts the skin barrier function. Prolonged exposure of human skin to UVB light is well known to trigger severe skin lesions such as cell death and carcinogenesis. Haloarcula vallismortis is a halophilic microorganism isolated from the Dead Sea, Its growth characteristics have not been studied in detail yet. It generally grows at salinity more than 10%, but the actual growth salinity usually ranges between 20 to 25%. Because H. vallismortis is found mainly in saltern or salt lakes, there could exist defense mechanisms against strong sunlight. One of them is generation of additional ATP using halorhodopsin which absorbs photons and produces energy by potential difference formed by opening the chloride ion channel. It often shows a color of pink or red because of their high content of carotenoid pigments and it is considered to act as a defense mechanism against intense UV irradiation. In this study, the anti-inflammatory effect of the halophilic microorganism, H. vallismortis, extract was investigated. It was found that H. vallismortis extract had protective effect on DNA damage induced by UV irradiation. These results suggest that the extract of halophilic bacterium, H. vallismortis could be used as a bio-sunscreen or natural sunscreen which ameliorate the harmful effects of UV light with its anti-inflammatory and DNA protective properties.

• Tuberculosis and Respiratory Diseases
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• v.45 no.4
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• pp.861-869
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• 1998

Backgrounds: The injury of a tissue results in the infalmmation, and the imflammed tissue is replaced by the normal parenchymal cells during the process of repair. But, constitutional or repetitive damage of a tissue causes the deposition of collagen resulting in the loss of its function. These lesions are found in the lung of patients with idiopathic pulmonary fibrosis, complicated fibrosis after diffuse alveolar damage (DAD) and inorganic dust-induced lung fibrosis. The tissue from lungs of patients undergoing episodes of active and/or end-stage pulmonary fibrosis shows the accumulation of inflammatory cells, such as mononuclear cells, neutrophils, mast cells and eosinophils, and fibroblast hyperplasia. In this regard, it appears that the inflammation triggers fibroblast activation and proliferation with enhanced matrix synthesis, stimulated by inflammatory mediators such as interleukin-1 (IL-1) and/or tumor necrosis factor (TNF). It has been well known that TGF-$\beta$ enhance the proliferation of fibroblasts and the production of collagen and fibronectin, and inhibit the degradation of collagen. In this regard, It is likely that TGF-$\beta$ undergoes important roles in the pathogenesis of pulmonary fibrosis. Nevertheless, this single cytokine is not the sole regulator of the pulmonary fibrotic response. It is likely that the balance of many cytokines including TGF-$\beta$, IL-1, IL-6 and TNF-$\alpha$ regulates the pathogenesis of pulmonary fibrosis. In this study, we investigate the interaction of TGF-$\beta$, IL-1$\beta$, IL-6 and TNF-$\alpha$ and their effect on the proliferation of fibroblasts. Methods: We used a human fibroblast cell line, MRC-5 (ATCC). The culture of MRC-5 was confirmed by immunofluorecent staining. First, we determined the concentration of serum in cuture medium, in which the proliferation of MRC-5 is supressed but the survival of MRC-5 is retained. Second, we measured optical density after staining the cytokine-stimulated cells with 0.5% naphthol blue black in order to detect the effect of cytokines on the proliferation of MRC-5. Result: In the medium containing 0.5% fetal calf serum, the proliferation of MRC-5 increased by 50%, and it was maintained for 6 days. IL-1$\beta$, TNF-$\alpha$ and IL-6 induced the proliferation of MRC-5 by 45%, 160% and 120%, respectively. IL-1$\beta$ and TNF-$\alpha$ enhanced TGF-$\beta$-induced proliferation of MRC-5 by 64% and 159%, but IL-6 did not affect the TGF-$\beta$-induced proliferation. And lNF-$\alpha$-induced proliferation of MRC-5 was reduced by IL-1$\beta$ in 50%. TGF-$\beta$, TNF-$\alpha$ and both induced the proliferation of MRC-5 to 89%, 135% and 222%, respectively. Conclusions: TNF-$\alpha$, TGF-$\beta$ and IL-1$\beta$, in the order of the effectiveness, showed the induction of MRC-5 proliferation of MRC-5. TNF-$\alpha$ and IL-1$\beta$ enhance the TGF-$\beta$-induced proliferation of MRC-5, but IL-6 did not have any effect TNF-$\alpha$-induced proliferation of MRC-5 is diminished by IL-1, and TNF-$\alpha$ and TGF-$\beta$ showed a additive effect.