• Korean Journal of Plant Resources
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• v.30 no.2
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• pp.144-151
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• 2017

This study examined the anti-inflammatory and whitening effects of Amaranth (Amaranthus spp L.) seed extract. Amaranthus spp L. seeds were extracted using 70% ethanol and then fractionated sequentially with n-hexane, dichloromethan, ethyl acetate and butanol. For the study of anti-inflammatory activity in RAW 264.7 cells, EtOAc fraction of Amaranthus spp L. seeds significantly inhibited nitrogen oxide production as well as the protein level of iNOS. Furthermore, EtOAc fraction of Amaranthus spp L. seeds inhibited expression of $TNF-{\alpha}$, PGE2 and the protein level of COX-2 in a dose-dependent manner. Inaddition, the tyrosinase inhibitory activities of the Amaranthus spp L. seed 70% ethanol extract and subfractions were also measured to see if these extracts can be used as an ingredient for whitening cosmetics. Tyrosinase is an oxidase that is a rate-limiting enzyme for controlling the production of melanin. Therefore, tyrosinase inhibitors have become increasingly important in cosmetics and medical products with regards to hyperpigmentation. EtOAc fraction of Amaranthus spp L. seeds showed mushroom tyrosinase inhibitory activity in a dose-dependent manner. This activity was more potent than that of a positive control cynandione A. These results suggest that Amaranthus spp L. seeds may be a valuable natural ingredient for the food and cosmetics industries.

• Journal of Mushroom
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• v.19 no.3
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• pp.225-233
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• 2021

In this study, we evaluated the anti-inflammatory effect of extract from Cudrania tricuspidata twig sawdust fermented with Ganoderma lucidum mycelium. Fermented Cudrania tricuspidata twig sawdust extracted with 70% ethanol and elucidated the potential signaling pathway in lipopolysaccharide (LPS)-induced RAW264.7 cells. Fermented Cudrania tricuspidata twig sawdust inhibits LPS-stimulated nitric oxide (NO) production without affecting cell viability in a dose-dependent manner and production of LPS-induced pro-inflammatory cytokines such as interleukin (IL)-1β, tumor necrosis factor (TNF)-α and prostaglandin2 (PGE₂). Fermented Cudrania tricuspidata twig sawdust also suppressed the expression of the pro-inflammatory mediators such as inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in LPS-stimulated RAW264.7 cells. Moreover, Fermented Cudrania tricuspidata twig sawdust significantly attenuated LPS-induced IkappaB (IκB) degradation and suppressed nuclear factor kappa B (NF-κB) nuclear translocation. These results suggest that fermented Cudrania tricuspidata twig sawdust may have great potential for the development of anti-inflammatory agent.

• Journal of the Korean Chemical Society
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• v.51 no.3
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• pp.251-257
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• 2007

The Tumor necrosis factor-α, (TNF-α), is involved in the pathogenesis of multiple sclerosis and contributes to the degeneration of oligodendrocytes as well as neurons. Nicotine has been found to have immunosuppressive and inflammation-suppressing effects. Astrocytes, the major glial cells in the CNS, are capable of producing TNF-α at both the mRNA and protein levels in response to interleukin-1 (IL-1) or TNF-α. Nicotine has been shown to influence glial cell functions. To order to explore the role of astrocytes in the production of TNF-α, astrocytes were pretreated with nicotine and are stimulated with IL-1β to determine their effects on TNF-α production. The results are as follows. Cytotoxic effects of nicotine on human fetal astrocytes were noted above 10 μg/ml of nicotine. The effect of IL-1β on TNF-α mRNA expression in primary cultured human fetal astrocytes was maximal at 2 h after IL- 1β(100 pg/ml) treatment. Human fetal astrocytes were pretreated with 0.1, 1, and 10 μg/ml of nicotine and then stimulated with IL-1β (100 pg/ml) for 2 h. The inhibitory effect of nicotine on expressions of TNF-α mRNA in human fetal astrocytes with pretreated 0.1 μg/ml of nicotine is first noted at 8 hr, and the inhibitory effect is maximal at 12 h. The inhibitory effect at 1 μg/ml of nicotine is inhibited maximal at 24 h. Nicotine at 0.1, 1 and 10 μg/ml concentrations significantly inhibits IL-1β-induced NF-κB activation. Collectively, this study indicates that nicotine might inhibit the expression of TNF-α in activated human fetal astrocytes.

• Journal of the Society of Cosmetic Scientists of Korea
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• v.50 no.3
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• pp.271-278
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• 2024

The human skin is an organ that protects the body from physical and chemical factors. The skin is the largest and most massive of the body's organs and is composed of the epidermis, dermis, and subcutaneous tissue. Constant UV exposure to the skin can cause DNA damage, oxidation of proteins, and contribute to adult diseases. Nypa fruticans Wurmb (NF), rich in phytochemicals (polyphenols and flavonoids), has been traditionally used for treating respiratory and other diseases. This study investigated the effects of NF ethyl acetate fraction (ENF) on DNA damage healing and inhibition of wrinkle-related factors in UVB-stimulated Hs68 cells. Westernblotting was used to assess the expression of DNA damage-related proteins and wrinkle-related protein factors. In addition, the wound recovery capability of ENF was confirmed through wound-healing experiments. ENF significantly suppressed the expression of DNA damage-related proteins Phosphorylated H2AX (γ-H2AX), checkpoint kinase 2 (Chk2), protein53 (p53), and Phosphorylated protein53 (p-p53). Furthermore, ENF inhibited the expression of wrinkle-related proteins matrix metalloproteinase-1 (MMP-1), matrix metalloproteinase-3 (MMP-3), and matrix metalloproteinase-9 (MMP-9). High concentrations of ENF also enhanced wound healing in Hs68 cells. ENF is thought to have the potential to heal DNA damage by significantly suppressing the expression of γ-H2AX, Chk2, p53, and p-p53, as well as to inhibit wrinkle formation by suppressing the expression of MMP-1, MMP-3, and MMP-9. These results suggest that ENF can be used as a natural resource to suppress skin damage caused by UVB by regulating the γ-H2AX, Chk2, p53, and MMP pathways in Hs68 cells induced by UVB.

• Journal of Acupuncture Research
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• v.27 no.4
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• pp.39-53
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• 2010

목적 : 퇴행성 관절염은 염증성 사이토카인인 IL-$1\beta$에 의해 연골관절이 파괴되고 이로 인해 염증성 사이토카인이 더욱 증가하는 질환이다. 퇴행성 관절염을 치료하기 위해서는 연골 파괴를 가속화시키는 catabolic cytokines의 활성을 줄이고, 성장인자인 anabolic factor의 활성을 증가시는 연골 보호 작용이 있어야 한다. 본 연구에서는 독활 승마 처방(OAH19T)이 catabolic/anabolic 대사 조절에 어떤 영향을 미치는지와 그 신호 전달 기전에 대해 연구하였다. 또한 OAH19T를 구성하는 단미재 및 임상에서 사용되는 COX-2 inhibitor인 Celebrex(CEL)와 효능을 비교 실험하였다. 방법 : 배양된 세포에 IL-$1\beta$로 자극한 후 (1) glycosaminoglycan(GAG)의 분해 억제 정도, (2) OAH19T와 CEL에 대하여 MMP-1과 MMP-3의 유전자 발현 및 활성 억제, (3) Aggrecan 및 Aggrecanases의 유전자 발현 및 활성 억제, (4) OAH19T의 growth factor의 조절 능력, (5) MAPK pathway 등을 RT-PCR(reverse transcriptase-polymerase chain reaction), ELISA(Enzyme-linked immunosorbent assay), western blot, viability 측정을 통해 검증했다. 결과 : 사람 관절 세포에서 (1) 독활 승마 각각의 단미재, 임상에서 사용중인 셀레콕시브(CEL), 조인스보다 실험 약물(OAH19T)이 저농도에서 GAG 분해 억제 효과가 우수하였고, 부탄올로 분획한 OAH19B와는 동등한 효과를 보였다. (2) OAH19T는 IL-$1\beta$에 의하여 활성화된 MMP-1과 MMP-3의 발현을 모두 억제하였으나, CEL은 MMP-1의 발현은 억제하였으나 MMP-3의 발현은 억제하지 못하였다. (3) OAH19T는 IL-$1\beta$에 의하여 손상된 Aggrecan을 회복시켰으며 이는 활성화된 Aggrecanase-1과 Aggrecanase-2를 억제시킴으로써 나타난 결과이다. 그러나 CEL의 경우, 손상된 Aggrecan을 회복시키지 못하였다. (4) 배양된 세포는 IL-$1\beta$에 의하여 TGF-$\beta$II및 TGF-$\beta$ receptor II의 발현이 억제되었으나, OAH19T는 TGF-$\beta$II및 TGF-$\beta$ receptor II의 발현을 회복시켜 OAH19T가 anabolic한 조절능력이 있음을 시사한다. 그러나 CEL의 경우 growth factor에 대한 조절 능력이 없었다. (5) 대사 조절 작용에 대한 기전으로서 MAPK pathway에 대해서 연구한 결과 IL-$1\beta$에 의하여 유도된 pERK, pp38 kinase의 활성은 억제하였고, pJNK의 활성은 변하지 않았다. 또한 OAH19T는 연골 세포에 독성이 없었으며 IL-$1\beta$에 의해 유도된 세포 증식만을 억제시켰다. 이 결과로, OAH19T가 OA chondrocyte의 탈분화 및 세포 고사를 억제하여 연골보호 및 회복 효과가 있음을 알 수 있었다. 결론 : OAH19T는 이를 구성하는 단미재 및 CEL보다 연골보호 효과가 월등하였고, 이러한 연골보호 효과는 catabolic cytokines/growth factors의 균형으로 대사조절을 통해 연골세포의 탈분화 및 세포 고사를 억제하여 연골보호 및 회복 효과가 있음을 알 수 있었다.

• Journal of dental hygiene science
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• v.9 no.4
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• pp.427-433
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• 2009

Nuclear factor I-C (NFI-C) null mice demonstrated aberrant odontoblast differentiation and abnormal dentin formation. In order to elucidate the mechanisms responsible for these changes, we evaluated the expression of dentin matrix gene after over-expression and inactivation of NFI-C in MDPC-23 cells by reverse transcription-polymerase chain reaction (RT-PCR) analysis. Collagen type I (Col I), osteocalcin (OC), and dentin sialophosphoprotein (DSPP) expression was decreased after inactivation of NFI-C. However, bone sialoprotein (BSP) expression was dramatically increased after inactivation of NFI-C. ALP and DMP4 expression was not changed after inactivation of NFI-C. The expression of alkaline phoshatase (ALP) and dentin matrix protein 4 (DMP4) was increased after over-expression of NFI-C, while Col I, OC, DSPP, and BSP expression was decreased. These findings suggest that odontoblasts after loss of NFI-C lost the phenotype of odontoblasts and acquired those of osteoblasts.

• Journal of Industrial Convergence
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• v.21 no.8
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• pp.69-74
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• 2023

This paper was conducted to examine the effect of Brussels Sprouts Extract on the inhibition of pro-inflammatory cytokines. The inflammatory response is manifested by mediators such as reactive oxygen species and inflammatory cytokines such as TNF-α, IL-1β, and IL-8. Therefore, this paper examined the toxicity to cells using the MTS assay, stimulated RAW264.7 macrophages with lipopolysaccharide (LPS), and stimulated reactive oxygen species such as NO and TNF-α, IL-1β, and IL-8. Inhibition of inflammatory cytokines after treatment with 10 mg/mL, 100 mg/mL, and 1000 mg/mL of Brussels Sprouts Extract was investigated. As a result of the experiment, Brussels Sprouts Extract inhibited NO production, TNF-α and IL-8 in a concentration-dependent manner without cytotoxicity, and showed significant inhibition especially at a concentration of 1000 mg/mL. Brussels Sprouts Extract, which inhibits the production of inflammatory cytokines, suggests the possibility of reducing inflammatory response and controlling inflammation, and can be seen as providing potential as a health functional food or prevention and treatment of inflammation.

• Journal of radiological science and technology
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• v.39 no.3
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• pp.443-449
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• 2016

In the present study, whether squalene treatment relives inflammatory reactions induced by Candida albicans was checked. The experiment was conducted in vivo using seven experimental animals (ICR mice) per experimental group. Among C. albicans-induced inflammatory factors, TNF-${\alpha}$, IL-6, and NO were observed using the ELISA kits method. Through the experiment, the following conclusions were obtained. 1. In the group infected with C. albicans, it could be identified that squalene treatment was inducing NO generation in renal tissues both on the 1st and 3rd days (p < 0.05). 2. In the group pre-treated(intraperitoneal administration) with SQ (80ml/kg) once per day for seven days and infected with C. albicans, it could be identified that squalene treatment was inducing TNF-${\alpha}$ generation in renal tissues only on the 3rd day(p < 0.05). 3. In the group pre-treated(intraperitoneal administration) with SQ (80ml/kg) once per day for seven days and infected with C. albicans, it could be identified that squalene treatment was inducing IL-6 generation in renal tissues only on the 3rd day(p < 0.05). In conclusion, it could be seen that for squalene to suppress C. albicans-induced inflammatory factors, preemptively supplying SQ should be effective. Therefore, effects for recovery from C. albicans-induced immunodepression can be expected from SQ treatment.

• Journal of the Society of Cosmetic Scientists of Korea
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• v.46 no.1
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• pp.11-22
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• 2020

In this study, we investigated anti-pigmentation effect of a hexapeptide. The peptide significantly reduced melanin contents and inhibited tyrosinase activity in a dose-dependent manner, in which tyrosinase is a key enzyme in melanogenesis. The peptide also significantly reduced the expression levels of tyrosinase (TYR), tyrosinase-related protein 1 (TYRP1) and their upstream transcription factor, microphthalmia-associated transcription factor (MITF). Furthermore, the peptide suppressed the phosphorylation level of cAMP-response element binding protein (CREB), a transcription factor of MITF, and increased the phosphorylation level of extracellular signal-regulated kinase (ERK), a kinase mediates MITF phosphorylation and proteasomal degradation. The peptide significantly inhibited the expression of Rab27A, Melanophilin, and MyosinVa, the components of motor complex involved in intracellular movement of melanosome. These results suggest that Hexapeptide could be used as an effective whitening agent that has inhibitory effect on melanin production and melanosome transport by regulating expression and degradation of MITF in melanocytes.

• Korean Journal of Clinical Laboratory Science
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• v.52 no.4
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• pp.417-424
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• 2020

This study aimed to explore the effects of brain-derived neurotrophic factor (BDNF), produced by engineered immortalized mesenchymal stem cells (imMSC), on lower urinary tract symptoms (LUTS) in a rat model with neurogenic bladder (NB). Forty-eight Sprague-Dawley (SD) rats were randomly divided into the following groups: Sham control, LUTS, LUTS+imMSC (treated with immortalized MSC), and LUTS+BDNF-eMSC (treated with BDNF-expressing MSC) groups. LUTS was induced by a crush injury to the major pelvic ganglion (MPG). Bladder function was tested under anesthesia, and bladder tissue strips were collected thereafter for contractility test and western blot analysis. Western blot results showed that the expression of both Angiopoietin 1 (Ang 1) and platelet-derived growth factor (PDGF) increased with MSC injection. The effect of treatment with BDNF-eMSC on LUTS was also evaluated, and the results were found to be better than those with imMSC (P<0.05). BDNF-eMSC prevented fibrosis in the bladder tissue and significantly reduced caspase-3 levels. In conclusion, high expression of BDNF in vivo resulted in recovery of bladder function and contractility, along with the inhibition of apoptosis in a rat model.