https://repository.kopri.re.kr/handle/201206/5116 2026-04-03T18:18:42Z https://repository.kopri.re.kr/handle/201206/6126 Title: Ramalin Isolated from Ramalina Terebrata Attenuates Atopic Dermatitis-like Skin Lesions in Balb/c Mice and Cutaneous Immune Responses in Keratinocytes and Mast Cells Authors: Park, Hye-Jin; Pyo, Suhkneung; Lee, Hong Kum; Yim, Joung Han; Jang, Yeon Jeong Abstract: Atopic dermatitis (AD) is a chronic inflammatory skin disease that involves eczematous skin lesions with pruritic erythematous papules. In this study, we investigated the mitigating effects of ramalin, a component of the Antarctic lichen Ramalina terebrata against AD in vivo and in vitro. Oral administration of ramalin lessened scratching behaviors and significantly reduced both serum immunoglobulin E and IL-4 levels, and mRNA levels of IL-4 and IL-10 in AD-induced Balb/c mice. In vitro, treatment with ramalin produced significantly less inflammatory chemokines and cytokines, including TARC, MCP-1, RANTES, and IL-8 in TNF-α-stimulated HaCaT cells. In addition, ramalin inhibited the activation of nuclear factor-kappa B as well as the phosphorylation of mitogen-activated protein kinases (MAPK). Furthermore, ramalin treatment resulted in decreased production of β-hexosaminidase and proinflammatory cytokines IL-4, IL-6, and TNF-α in 2,4 dinitrophenyl-human serum albumin-stimulated RBL-2H3 cells through blocking MAPK signaling pathways. The results suggest that ramalin modulates the production of immune mediators by inhibiting the nuclear factor-kappa B and MAPK signaling pathways. Taken together, ramalin effectively attenuated the development of AD and promoted the mitigating effects on Th2 cell-mediated immune responses and the production of inflammatory mediators in mast cells and keratinocytes. Thus, ramalin may be a potential therapeutic agent for AD. 2016-01-01T00:00:00Z https://repository.kopri.re.kr/handle/201206/6181 Title: Inhibition of VCAM-1 expression on mouse vascular smooth muscle cells by lobastin via downregulation of p38, ERK 1/2 and NF-κB signaling pathways Authors: Lee, Kyoungran; Pyo, Suhkneung; Lee, Hong Kum; Yim, Joung Han Abstract: Atherosclerosis is a chronic inflammatory disease, the progression of which is associated with the increased expression of cell adhesion molecules on vascular smooth muscle cells (VSMCs). Lobastin is a new pseudodepsidone isolated from Stereocaulon alpinum, Antarctic lichen, which is known to have antioxidant and antibacterial activities. However, the nature of the biological effects of lobastin still remains unclear. In the present study, we examine the effect of lobastin on the expression of vascular cell adhesion molecules (VCAM-1) induced by TNF-a in the cultured mouse VSMC cell line, MOVAS-1. Pretreatment of VSMCs for 2 h with lobastin (0.1？10 lg/ ml) concentration-dependently inhibited TNF-a-induced protein expression of VCAM-1. Lobastin also inhibited TNF-a-induced production of intracellular reactive oxygen species (ROS). Lobastin abrogated TNF-a-induced phosphorylation of p38 and ERK 1/2, but not JNK, and also inhibited TNF-a-induced NK-jB activation. In addition, lobastin suppressed TNF-a-induced IjB kinase activation, subsequent degradation of IjBa and nuclear translocation of p65 NF-jB. Our results indicate that lobastin downregulates the TNF-a-mediated induction of VCAM-1 in VSMC by inhibiting the p38, ERK 1/2 and NF-jB signaling pathways and intracellular ROS generation. Thus, lobastin may be an important regulator of inflammation in the atherosclerotic lesion and a novel therapeutic drug for the treatment of atherosclerosis. 2016-01-01T00:00:00Z https://repository.kopri.re.kr/handle/201206/7340 Title: Enhanced production of protease by Pseudoalteromonas arctica PAMC 21717 via statistical optimization of mineral components and fed-batch fermentation Authors: Han, Se Jong; Yim, Joung Han; Park, Ha Ju; Kim, Dockyu; 김성희; Park, Heeyong Abstract: The objective of this study was to statistically optimize the mineral components of the nutritional medium required for enhancing the production of a cold-active extracellular serine-type protease, W-Pro21717, by the Antarctic bacterium Pseudoalteromonas arctica PAMC 21717. Skim milk was identified as the major efficient inducer. Among the 12 components included in the unoptimized medium, skim milk, NaCl, Na2SO4, Fe(C6H5O7) (ferric citrate), and KCl were determined, by the Plackett-Burman and Box-Behnken design, to have a major effect on W-Pro21717 production. Fed-batch fermentation (5 L scale) using the mineral-optimized medium supplemented with concentrated skim milk (critical medium component) resulted in a W-Pro21717 activity of 53.4 U/L, a 15-fold increment in production over that obtained using unoptimized flask culture conditions. These findings could be applied to scale-up the production of cold-active protease. 2016-01-01T00:00:00Z https://repository.kopri.re.kr/handle/201206/6125 Title: Ramalin-Mediated Apoptosis Is Enhanced by Autophagy Inhibition in Human Breast Cancer Cells Authors: Lee, Eunyoung; Pyo, Suhkneung; Lee, Hong Kum; Yim, Joung Han; Chung Gi Lee Abstract: Breast cancer, the most commonly diagnosed cancer in women worldwide, is treated in various ways. Ramalin is a chemical compound derived from the Antarctic lichen Ramalina terebrata and is known to exhibit antioxidant and antiinflammatory activities. However, its effect on breast cancer cells remains unknown. We examined the ability of ramalin to induce apoptosis and its mechanisms in MCF-7 and MDA-MB-231 human breast cancer cell lines. Ramalin inhibited cell growth and induced apoptosis in both cell lines in a concentration-dependent manner. By upregulating Bax and downregulating Bcl-2, ramalin caused cytochrome c and apoptosis-inducing factor to be released from the mitochondria into the cytosol, thus activating the mitochondrial apoptotic pathway. In addition, activated caspase-8 and caspase-9 were detected in both types of cells exposed to ramalin, whereas ramalin activated caspase-3 only in the MDA-MB-231 cells. Ramalin treatment also increased the levels of LC3-II and p62. Moreover, the inhibition of autophagy by 3-methyladenine or Atg5 siRNA significantly enhanced ramalin-induced apoptosis, which was accompanied by a decrease in Bcl-2 levels and an increase in Bax levels. Therefore, autophagy appears to be activated as a protective mechanism against apoptosis in cancer cells exposed to ramalin. These findings suggest that ramalin is a potential anticancer agent for the treatment of patients with non-invasive or invasive breast cancer. 2016-01-01T00:00:00Z