• Journal of Ginseng Research
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• 제44권1호
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• pp.115-122
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• 2020

Background: In aged skin, degradation of collagen fibers, which occupy the majority of the extracellular matrix in the dermis, and changes of aquaporin 3 (AQP3) and skin constituents, such as hyaluronic acid and ceramide, cause wrinkles and decrease skin moisturization to contribute to dryness and lower elasticity skin. Red ginseng (RG) is used as a cosmetic and food material and is known to protect from UVB-induced cell death, increase skin hydration, prevent wrinkles, and have an antioxidative effect. But, in general, RG used as a material is the soluble liquid portion in the solvent, and the part that is not soluble in the solvent is discarded. Thus, we made the whole RG into microgranulation and dispersed in water to produce gel form for using entire RG, and it was named red ginseng NaturalGEL (RG NGEL). Methods: RG NGEL was investigated for matrix metalloproteinases inhibitory activity, induction of Type I collagen, AQP3, hyaluronan synthetase 2, serine palmitoyl transferase, ceramide synthase 3, and filaggrin expression and compared with RG water extract. Results: RG NGEL reduced the levels of UV-induced matrix metalloproteinases and increased Type I collagen in human fibroblast cells and upregulated AQP3, hyaluronan synthetase 2, serine palmitoyl transferase, ceramide synthase 3, and filaggrin expressions in human keratinocytes compared with RG water extract. Conclusion: RG NGEL has the potential as an effective reagent for antiaging cosmetics to improve wrinkle formation and skin hydration.

• Molecules and Cells
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• 제38권12호
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• pp.1096-1104
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• 2015

Particulate $matter_{2.5}$ ($PM_{2.5}$) is notorious for its strong toxic effects on the cardiovascular, skin, nervous, and reproduction systems. However, the molecular mechanism by which $PM_{2.5}$ aggravates disease progression is poorly understood, especially in a water-soluble state. In the current study, we investigated the putative physiological effects of aqueous $PM_{2.5}$ solution on lipoprotein metabolism. Collected $PM_{2.5}$ from Seoul, Korea was dissolved in water, and the water extract (final 3 and 30 ppm) was treated to human serum lipoproteins, macrophages, and dermal cells. $PM_{2.5}$ extract resulted in degradation and aggregation of high-density lipoprotein (HDL) as well as low-density lipoprotein (LDL); apoA-I in HDL aggregated and apo-B in LDL disappeared. $PM_{2.5}$ treatment (final 30 ppm) also induced cellular uptake of oxidized LDL (oxLDL) into macrophages, especially in the presence of fructose (final 50 mM). Uptake of oxLDL along with production of reactive oxygen species was accelerated by $PM_{2.5}$ solution in a dose-dependent manner. Further, $PM_{2.5}$ solution caused cellular senescence in human dermal fibroblast cells. Microinjection of $PM_{2.5}$ solution into zebrafish embryos induced severe mortality accompanied by impairment of skeletal development. In conclusion, water extract of $PM_{2.5}$ induced oxidative stress as a precursor to cardiovascular toxicity, skin cell senescence, and embryonic toxicity via aggregation and proteolytic degradation of serum lipoproteins.

• 대한의용생체공학회:의공학회지
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• 제27권5호
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• pp.218-223
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• 2006

We examined the effects of ${\beta}$-glucan-reinforced PLGA film and scaffold on HDFs (human dermal fibroblast) attachment and proliferation. The PLGA films were prepared by simple solvent-casting method. The prepared films were grafted with $(1{\to}3)(1{\to}6)-{\beta}-glucan$ in various ratios after plasma treatment on surface. The surface of the film was characterized by contact angle measurement, scanning electron microscope (SEM), and Fourier-transform infrared spectrophotometer (FT-IR). The amount of $(1{\to}3)(1{\to}6)-{\beta}-glucan$ in the prepared film was indirectly determined by phenol-sulfuric acid method. The HDFs (Human dermal fibroblasts) were used to evaluate the cell attachment and proliferation on PLGA specimens before and after plasma/${\beta}-glucan$ treatment. The result showed that the plasma treated groups exhibited more mont of ${\beta}-glucan$ might be grafted than the non plasma treated groups. Cell attachment was significantly enhanced in the plasma/${\beta}-glucan$ grafted group after 4 hours incubation (p<0.05) due to the improved hydrophilicity and cytoactivity effect of the ${\beta}-glucan$. The cell proliferation of plasma/${\beta}-glucan$ (2mg/ml) grafted group was the highest rate among the groups (p<0.05).

• 대한안과학회지
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• 제59권11호
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• pp.1056-1061
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• 2018

목적: 발프로익산이 배양된 인체 테논낭 섬유아세포의 생존에 미치는 영향에 대해 알아보고자 하였다. 대상과 방법: 일차배양한 섬유아세포에 0, 0.25, 0.5, 1.0 mM 발프로익산과 0, 1.0, $2.5{\mu}g/mL$ 미토마이신 C에 각각 또는 동시에 5일간 노출시킨 후 MTT (3-[4, 5-dimethylthiazol-2-yl]-2, 5-diphenyltetrazolium bromide) assay를 이용하여 세포의 생존을 측정하였고, annexin-V/propidium iodide 이중염색 후 유세포 분석을 이용하여 세포고사의 정도를 측정하였다. 결과: 발프로익산은 농도에 비례하여 섬유아세포의 생존을 유의하게 저하시켰으며, 미토마이신 C를 추가한 경우 섬유아세포의 생존을 더욱 저하시켰다. 두 약제 모두 섬유아세포의 세포고사를 유발하였으나 발프로익산은 미토마이신 C에 비해 세포고사를 적게 유발하였다. 결론: 발프로익산은 섬유아세포의 생존을 저하시키며 세포고사를 유발한다. 또한 미토마이신 C를 병용한 경우 섬유아세포에 대한 항증식효과가 더 나타날 것으로 생각된다.

• Nutrition Research and Practice
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• 제13권2호
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• pp.95-104
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• 2019

BACKGROUND/OBJECTIVES: Inflammatory Bowel Disease (IBD) has rapidly escalated in Asia (including Korea) due to increasing westernized diet patterns subsequent to industrialization. Factors associated with endoplasmic reticulum (ER) stress are demonstrated to be one of the major causes of IBD. This study was conducted to investigate the effect of Lycium barbarum (L. barbarum) on ER stress. MATERIALS/METHODS: Mouse embryonic fibroblast (MEF) cell line and polarized Caco-2 human intestinal epithelial cells were treated with crude extract of the L. chinense fruit (LF). Paracellular permeability was measured to examine the effect of tight junction (TJ) integrity. The regulatory pathways of ER stress were evaluated in MEF knockout (KO) cell lines by qPCR for interleukin (IL) 6, IL8 and XBP1 spliced form (XBP1s). Immunoglobulin binding protein (BiP), XBP1s and CCAAT/enhancer-binding homologous protein (CHOP) expressions were measured by RT-PCR. Scanning Ion Conductance Microscopy (SICM) at high resolution was applied to observe morphological changes after treatments. RESULTS: Exposure to LF extract strengthened the TJ, both in the presence and absence of inflammation. In polarized Caco-2 pretreated with LF, induction in the expression of proinflammatory marker IL8 was not significant, whereas ER stress marker XBP1s expression was significantly increased. In wild type (wt) MEF cells, IL6, CHOP and XBP1 spliced form were dose-dependently induced when exposed to $12.5-50{\mu}g/mL$ extract. However, absence of XBP1 or $IRE1{\alpha}$ in MEF cells abolished this effect. CONCLUSION: Results of this study show that LF treatment enhances the barrier function and reduces inflammation and ER stress in an $IRE1{\alpha}$-XBP1-dependent manner. These results suggest the preventive effect of LF on healthy intestine, and the possibility of reducing the degree of inflammatory symptoms in IBD patients.

• Molecules and Cells
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• 제42권2호
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• pp.151-160
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• 2019

Ultraviolet (UV) radiation of the sunlight, especially UVA and UVB, is the primary environmental cause of skin damage, including topical inflammation, premature skin aging, and skin cancer. Previous reports show that activation of nuclear $factor-{\kappa}B$ ($NF-{\kappa}B$) in human skin fibroblasts and keratinocytes after UV exposure induces the expression and release of proinflammatory cytokines, such as interleukin-1 (IL-1) and tumor necrosis $factor-{\alpha}$ ($TNF-{\alpha}$), and subsequently leads to the production of matrix metalloproteases (MMPs) and growth factor basic fibroblast growth factor (bFGF). Here, we demonstrated that TNFR2-SKEE and TNFR2-SKE, oligopeptides from TNF receptor-associated factor 2 (TRAF2)-binding site of TNF receptor 2 (TNFR2), strongly inhibited the interaction of TNFR1 as well as TNFR2 with TRAF2. In particular, TNFR2-SKE suppressed UVB- or $TNF-{\alpha}$-induced nuclear translocalization of activated $NF-{\kappa}B$ in mouse fibroblasts. It decreased the expression of bFGF, MMPs, and COX2, which were upregulated by $TNF-{\alpha}$, and increased procollagen production, which was reduced by $TNF-{\alpha}$. Furthermore, TNFR2-SKE inhibited the UVB-induced proliferation of keratinocytes and melanocytes in the mouse skin and the infiltration of immune cells into inflamed tissues. These results suggest that TNFR2-SKE may possess the clinical potency to alleviate UV-induced photoaging in human skin.

• 대한의생명과학회지
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• 제25권2호
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• pp.177-184
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• 2019

Mutations in leucine-rich repeat kinase 2 (LRRK2) are the most common genetic cause of Parkinson's disease (PD). LRRK2 contains a functional kinase and GTPase domains. A pathogenic G2019S mutation that is the most prevalent among the LRRK2 mutations and is also found in sporadic cases, increases its kinase activity. Therefore, identification of LRRK2 kinase substrates and the development of kinase inhibitors are under intensive investigation to find PD therapeutics. Several recent studies have suggested members of Rab proteins, a branch of the GTPase superfamily, as LRRK2 kinase substrates. Rab proteins are key regulators of cellular vesicle trafficking. Among more than 60 members of human Rab proteins, Rab3, Rab5, Rab8, Rab10, Rab12, Rab29, Rab35, and Rab43 have been identified as LRRK2 kinase substrates. However, most studies have used human embryonic kidney (HEK) 293T cells overexpressing LRRK2/Rab proteins or murine embryonic fibroblast (MEF) cells which are not relevant to PD, rather than neuronal cells. In this study, we tested whether Rab proteins are phosphorylated by LRRK2 in astroglia in addition to neurons. Among the various Rab substrates, we tested phosphorylation of Rab10, because of the commercial availability and credibility of the phospho-Rab10 (pRab10) antibody, in combination with a specific LRRK2 kinase inhibitor. Based on the results of specific LRRK2 kinase inhibitor treatment, we concluded that LRRK2 phosphorylates Rab10 in the tested brain cells such as primary neurons, astrocytes and BV2 microglial cells.

• Journal of Microbiology and Biotechnology
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• 제31권7호
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• pp.999-1010
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• 2021

Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous in the environment. They are highly toxigenic and carcinogenic. Probiotic bacteria isolated from fermented foods were tested to check their ability to degrade and/or detoxify PAHs. Five probiotic bacteria with distinct morphologies were isolated from a mixture of 26 fermented foods co-cultured with benzo(a)pyrene (BaP) containing Bushnell Haas minimal broth. Among them, B. velezensis (PMC10) significantly reduced the abundance of BaP in the broth. PMC10 completely degraded BaP presented at a lower concentration in broth culture. B. velezensis also showed a clear zone of degradation on a BaP-coated Bushnell Haas agar plate. Gene expression profiling showed significant increases of PAH ring-hydroxylating dioxygenases and 4-hydroxybenzoate 3-monooxygenase genes in B. velezensis in response to BaP treatment. In addtion, both live and heat-killed B. velezensis removed BaP and naphthalene (Nap) from phosphate buffer solution. Live B. velezensis did not show any cytotoxicity to macrophage or human dermal fibroblast cells. Live-cell and cell-free supernatant of B. velezensis showed potential anti-inflammatory effects. Cell-free supernatant and extract of B. velezensis also showed free radical scavenging effects. These results highlight the prospective ability of B. velezensis to biodegrade and remove toxic PAHs from the human body and suggest that the biodegradation of BaP might be regulated by ring-hydroxylating dioxygenase-initiated metabolic pathway.

• 치위생과학회지
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• 제21권4호
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• pp.227-232
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• 2021

Background: Cancer-associated fibroblasts (CAFs) are abundant in tumor microenvironments and interact with cancer cells to promote tumor proliferation in oral squamous cell carcinoma (OSCC). Cathepsin D (CTSD) is a soluble lysosomal aspartic endopeptidase involved in tumor proliferation and angiogenesis. In this preliminary study, we observed CTSD expression in OSCC and CAFs, postulating that CTSD might act as a bridge between OSCC and CAFs. Methods: Human epidermal keratinocytes (HEKs), OSCC, and immortalized human normal oral fibroblasts (hTERT-hNOFs) were used in this study. Additionally, we used hTERT-hNOFs transfected with an empty vector, WT (wild-type)-YAP (Yes-associated protein), and YAPS127A (YAP serine 127 to alanine). YAP127A hTERT-hNOFs activated fibroblasts similar to CAFs. To identify CTSD expression between OSCC and CAFs, conditioned medium (CM) was collected from each cell. Protein expression of CTSD was identified by western blotting. Results: To identify the expression of CTSD in fibroblasts stimulated by OSCC, we treated fibroblasts with CM from HEK and OSCC. Results indicated that hTERT-hNOFs with OSCC CM showed a weakly increased expression of CTSD compared to stimulation by HEK CM. This indicates that CAFs, YAPS127 hTRET-hNOFs, overexpress CTSD protein. HEK cells showed no CTSD expression, regardless of treatment with fibroblast CM, whereas OSCC highly expressed CTSD proteins compared with the CTSD expression in HEK cells. We also found that CTSD expression was unaffected by changes in transforming growth factor-β levels. Conclusion: This study proposes that CTSD might have potential as an interacting executor between OSCC and CAFs. Further studies are needed to investigate the role of CTSD in tumor and stromal cells.

• Journal of Ginseng Research
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• 제46권5호
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• pp.646-656
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• 2022

Background: In addition to its use as a health food, ginseng is used in cosmetics and shampoo because of its extensive health benefits. The ginsenoside, Rh2, is a component of ginseng that inhibits tumor cell proliferation and differentiation, promotes insulin secretion, improves insulin sensitivity, and shows antioxidant effects. Methods: The effects of Rh2 on cell survival, extracellular matrix (ECM) protein expression, and cell differentiation were examined. The antioxidant effects of Rh2 in UV-irradiated normal human dermal fibroblast (NHDF) cells were also examined. The effects of Rh2 on mitochondrial function, morphology, and mitophagy were investigated in UV-irradiated NHDF cells. Results: Rh2 treatment promoted the proliferation of NHDF cells. Additionally, Rh2 increased the expression levels of ECM proteins and growth-associated immediate-early genes in ultraviolet (UV)-irradiated NHDF cells. Rh2 also affected antioxidant protein expression and increased total antioxidant capacity. Furthermore, treatment with Rh2 ameliorated the changes in mitochondrial morphology, induced the recovery of mitochondrial function, and inhibited the initiation of mitophagy in UV-irradiated NHDF cells. Conclusion: Rh2 inhibits mitophagy and reinstates mitochondrial ATP production and membrane potential in NHDF cells damaged by UV exposure, leading to the recovery of ECM, cell proliferation, and antioxidant capacity.