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Methyl gallate from Acer barbinerve decreases melanin synthesis in Mel-Ab cells.
Kim, In Wook,jeong, Hyo-Soon,Kim, Jin Kyu,Lee, Jin-Koo,Kim, Hak Rim,Yun, Hye-Young,Baek, Kwang Jin,Kwon, Nyoun Soo,Park, Kyoung-Chan,Kim, Dong-Seok GOVI VERLAG GMBH 2015 PHARMAZIE Vol.70 No.1
<P>Methyl gallate (MG) was isolated from the bark of Acer barbinerve, which has traditionally been used in Oriental medicine. In the present study, we examined the effects of MG on melanin synthesis in Mel-Ab melanocyte cells. MG decreased melanin pigmentation in a concentration-dependent manner, but did not directly inhibit tyrosinase activity. Further analysis showed that MG had no effect on extracellular signal-regulated kinase (ERK) activation, but induced phosphorylation of glycogen synthase kinase (GSK)3β, which is known to increase β-catenin accumulation. Accordingly, the β-catenin level was increased by MG. However, a specific GSK3β inhibitor did not rescue the MG-induced inhibition of melanogenesis. Additionally, MG decreased the protein expression of microphthalmia-associated transcription factor (MITF) and tyrosinase, which regulate melanin synthesis. Based on these results, we conclude that MG inhibits melanogenesis by decreasing the expression of MITF and tyrosinase.</P>
( Sung Hwan Suh ),( Kyoung Nyoun Kim ),( Mi Kyoung Park ),( Duk Kyu Kim ),( Moon Kyu Lee ),( Jae Hyeon Kim ) 대한내과학회 2014 대한내과학회 추계학술발표논문집 Vol.2014 No.1
Background: To investigate the relationship between markers of overall glucose exposure, postprandial glucose excursions and glycemic variability in patients with type 2 diabetes mellitus (T2DM). Methods: Sixty three patients with T2DM (mean age of 56 years) were enrolled, and all wore a continuous glucose monitoring system (CGMS) for 72 hours. We investigated the interrelationships between markers of overall glucose exposure, markers of postprandial glucose excursions and glycemic variability parameters from a CGMS. Results: Spearman`s correlation analysis revealed a signifi cant correlation between all markers of overall glucose exposure and various parameters related to glucose excursion. Percent coeffi cient of variation (CV) showed the strongest correlation with the GA (r = 0.470, p < 0.01). In participants with HbA1c levels < 7.5% (n = 33), almost all of glycemic markers and glycemic variability parameters were signifi cantly correlated with each other. All postprandial glucose excursion parameters also showed signifi cant correlation with other glycemic markers. In participants with HbA1c levels < 7.5% (n = 33), all markers of overall glucose exposure showed signifi cant interrelationships with mean glucose, postprandial glucose excursion and glycemic variability parameters (except CV). However, in participants with HbA1c levels = 7.5% (n = 30), postprandial glucose excursion and glycemic variability parameters were not related with any chronic glycemic marker. Conclusions: The postprandial glucose excursions may explain the glycemic variability and the total glucose exposures in well-controlled diabetic participants.
Kim, Dong-Seok,Park, Seo-Hyoung,Kwon, Sun-Bang,Kwon, Nyoun Soo,Park, Kyoung-Chan Pharmaceutical Society of Great Britain 2010 Journal of pharmacy and pharmacology Vol.62 No.2
<P>Objectives Sphingolipids act as structural components in cell membranes, and form lipid intermediates that have functional roles as signalling molecules in various cellular processes. Our previous findings have suggested that sphingolipid metabolites are deeply involved in the regulation of melanogenic processes. In this study we aimed to examine sphingosylphosphorylcholine-mediated signalling pathways related to melanogenesis. Methods We determined the hypopigmenting effects and the related signalling pathways of sphingosylphosphorylcholine in Mel-Ab cells. In particular, we analysed the involvement of the G-protein-coupled receptor in sphingosylphosphorylcholine-induced MITF degradation. Key findings Western blotting revealed that sphingosylphosphorylcholine induced the activation of extracellular signal-regulated kinase (ERK), as well as Akt. Moreover, the specific Akt pathway inhibitor LY294002 blocked the hypopigmenting effect of sphingosylphosphorylcholine and abrogated the sphingosylphosphorylcholine-mediated down-regulation of microphthalmia-associated transcription factor (MITF), showing that the Akt pathway is involved in sphingosylphosphorylcholine-mediated melanin inhibition. Treatment with the proteasome inhibitor MG132 blocked the decrease in MITF by sphingosylphosphorylcholine, but sphingosylphosphorylcholine did not decrease the level of MITF mRNA, indicating that the reduction in the level of MITF results from MITF degradation. Furthermore, pre-incubation of Mel-Ab cells with pertussis toxin completely abolished the hypopigmenting effects and the activation of ERK and Akt by sphingosylphosphorylcholine, suggesting that the effects of sphingosylphosphorylcholine are mainly dependent on the G-protein-coupled receptor). Conclusions Together, these results suggest that sphingosylphosphorylcholine reduces melanin synthesis via pertussis toxin-sensitive ERK and Akt activation, and subsequent MITF degradation.</P>
Kim, Su Yeon,Hahn, Hoh-Gyu,Nam, Kee Dal,Park, Kyoung-Chan,Yun, Hye-Young,Baek, Kwang Jin,Kwon, Nyoun Soo,Kim, Dong-Seok Pharmaceutical Society of Great Britain 2011 Journal of pharmacy and pharmacology Vol.63 No.8
<P>We have investigated whether KHG25855 (2-cyclohexylamino-1,3-thiazole hydrochloride) affected melanogenesis in B16 mouse melanoma cells, and the mechanisms involved.</P>
Effects of Cervi cornus Colla (deer antler glue) in the reconstruction of a skin equivalent model.
Kim, Jandi,Jeong, Hyo-Soon,Li, Hailan,Baek, Kwang Jin,Kwon, Nyoun Soo,Yun, Hye-Young,Choi, Hye-Ryung,Park, Kyoung-Chan,Kim, Dong-Seok Springer-Verlag 2013 Archives of dermatological research Vol.305 No.1
<P>The aim of this study was to investigate the effects of Cervi cornus Colla (CCC) in the reconstruction of skin equivalent (SE). H&E staining showed that SE containing hyaluronic acid (HA) or HA and CCC had a thicker epidermis than the control SE. Immunohistochemical staining showed that p63 was mainly present at the basal layer of the epidermis in the HA and CCC model. Involucrin was obviously expressed in the upper layer of the epidermis in the HA and CCC model. Moreover, we observed that integrins α6 and β1 were strongly expressed along the basement membrane zone in the HA and CCC model, in which the dermis expressing type I collagen was more compact. In conclusion, our data indicate that CCC contributed to the formation of epidermis, basement membrane, and extracellular matrix in the reconstruction of SE and suggest that CCC may be a useful adjuvant in the reconstruction of SE.</P>
김잔디 ( Jandi Kim ),이해란 ( Hailan Li ),정효순 ( Hyo-soon Jeong ),윤혜영 ( Hye-young Yun ),백광진 ( Kwang Jin Baek ),권년수 ( Nyoun Soo Kwon ),최혜령 ( Hye-ryung Choi ),박경찬 ( Kyoung-chan Park ),김동석 ( Dong-seok Kim ) 대한화장품학회 2013 대한화장품학회지 Vol.39 No.1
피부 자극과 부식 검사에 사용되는 동물실험을 대체하기 위한 방법으로 인공피부가 개발되어 왔다. 최근에 본 연구진은 녹각교를 함유하는 새로운 인공피부를 구축하였다. 현재 연구에서는 녹각교를 포함하는 인공피부를 사용하여 물질의 독성도 검사를 수행하였다. 그리하여 sodium dodecylsulfate (SDS) 또는 sodium carbonate를 인공피부에 도포하였고 표피의 손상 정도를 H&E와 면역조직화학 염색을 통하여 평가하였다. 인공피부의 표피는 SDS와 sodium carbonate에 의해 농도 의존적으로 영향을 받았다. 더 나아가 이들 물질에 의하여 p63의 발현이 감소하였다. 그러므로 녹각교를 함유하는 인공피부는 동물실험을 대체할 수 있는 모델로써 사용될 수 있고 in vitro에서 자극과 부식 검사 시험법의 발전에 도움을 줄 것으로 예상된다. To substitute animal test, skin equivalents (SEs) have been developed for skin irritation and corrosion test. Recently, we have developed new SEs containing Cervi cornus Colla (CCC). In the present study, we used the SEs for cutaneous cytotoxicity test. Sodium dodecylsulfate (SDS) or sodium carbonate was applied to the SEs, and the epidermal damage by H&E and immunohistochemical stains was evaluated. Our results showed that SDS or sodium carbonate affected the epidermal part of SEs containing CCC in a dose-dependent manner and decreased the expression of p63. It is concluded that SEs containing CCC could be used for an alternative model of animal test and would be greatly helpful in the development of in vitro irritation and corrosion test.
KHG26792 Inhibits Melanin Synthesis in Mel-Ab Cells and a Skin Equivalent Model
Li, Hailan,Kim, Jandi,Hahn, Hoh-Gyu,Yun, Jun,Jeong, Hyo-Soon,Yun, Hye-Young,Baek, Kwang Jin,Kwon, Nyoun Soo,Min, Young Sil,Park, Kyoung-Chan,Kim, Dong-Seok The Korean Society of Pharmacology 2014 The Korean Journal of Physiology & Pharmacology Vol.18 No.3
The purpose of this study is to characterize the effects of KHG26792 (3-(naphthalen-2-yl(propoxy)methyl)azetidine hydrochloride), a potential skin whitening agent, on melanin synthesis and identify the underlying mechanism of action. Our data showed that KHG26792 significantly reduced melanin synthesis in a dose-dependent manner. Additionally, KHG26792 downregulated microphthalmia-associated transcription factor (MITF) and tyrosinase, the rate-limiting enzyme in melanogenesis, although tyrosinase was not inhibited directly. KHG26792 activated extracellular signal-regulated kinase (ERK), whereas an ERK pathway inhibitor, PD98059, rescued KHG26792-induced hypopigmentation. These results suggest that KHG26792 decreases melanin production via ERK activation. Moreover, the hypopigmentary effects of KHG26792 were confirmed in a pigmented skin equivalent model using Cervi cornus Colla (deer antler glue), in which the color of the pigmented artificial skin became lighter after treatment with KHG26792. In summary, our findings suggest that KHG26792 is a novel skin whitening agent.
Balcos, Marie Carmel,Kim, Su Yeon,Jeong, Hyo-soon,Yun, Hye-young,Baek, Kwang Jin,Kwon, Nyoun Soo,Park, Kyoung-chan,Kim, Dong-seok Springer Science and Business Media LLC 2014 Acta pharmacologica Sinica. Vol.35 No.4
<P>To investigate the effects of docosahexaenoic acid (DHA) on melanin synthesis and related regulatory mechanisms.</P>
The regulatory mechanism of melanogenesis by FTY720, a sphingolipid analogue
Lee, Ju Eun,Kim, Su Yeon,Jeong, Yun‐,Mi,Yun, Hye‐,Young,Baek, Kwang Jin,Kwon, Nyoun Soo,Park, Kyoung‐,Chan,Kim, Dong‐,Seok Blackwell Publishing Ltd 2011 Experimental dermatology Vol.20 No.3
<P><B>Abstract: </B> We previously reported that sphingosine‐1‐phosphate (S1P) decreases melanin synthesis via extracellular signal‐regulated protein kinase (ERK) activation and microphthalmia‐associated transcription factor (MITF) degradation. Although FTY720 is an S1P structural analogue, the effects of FTY720 on melanogenesis are not completely understood. Thus, we investigated the influence of FTY720 on melanin synthesis in a spontaneously immortalized mouse melanocyte cell line (Mel‐Ab). FTY720 inhibited melanin synthesis in a concentration‐dependent manner. Further, FTY720 has a different signal transduction mechanism to regulate melanogenesis from the S1P‐induced signalling pathway. Our results showed that FTY720 down‐regulated MITF and tyrosinase expression without ERK activation. MITF, the master regulator of pigmentation, is a target for the Wnt signalling pathway, including glycogen synthase kinase 3β (GSK3β) and β‐catenin. Thus, the influence of FTY720 on GSK3β and β‐catenin was further investigated. Decreased MITF and tyrosinase were associated with a reduction of β‐catenin protein and mRNA levels. Decreased β‐catenin expression by FTY720 may down‐regulate expression of MITF, which finally reduces melanin synthesis.</P>
KHG26792 Inhibits Melanin Synthesis in Mel-Ab Cells and a Skin Equivalent Model
Hailan Li,Jandi Kim,Hoh-Gyu Hahn,Jun Yun,Hyo-Soon Jeong,Hye-Young Yun,Kwang Jin Baek,Nyoun Soo Kwon,Young Sil Min,Kyoung-Chan Park,Dong-Seok Kim 대한생리학회-대한약리학회 2014 The Korean Journal of Physiology & Pharmacology Vol.18 No.3
The purpose of this study is to characterize the effects of KHG26792 (3-(naphthalen-2-yl(propoxy) methyl)azetidine hydrochloride), a potential skin whitening agent, on melanin synthesis and identify the underlying mechanism of action. Our data showed that KHG26792 significantly reduced melanin synthesis in a dose-dependent manner. Additionally, KHG26792 downregulated microphthalmiaassociated transcription factor (MITF) and tyrosinase, the rate-limiting enzyme in melanogenesis, although tyrosinase was not inhibited directly. KHG26792 activated extracellular signal-regulated kinase (ERK), whereas an ERK pathway inhibitor, PD98059, rescued KHG26792-induced hypopigmentation. These results suggest that KHG26792 decreases melanin production via ERK activation. Moreover, the hypopigmentary effects of KHG26792 were confirmed in a pigmented skin equivalent model using <em>Cervi cornus Colla</em> (deer antler glue), in which the color of the pigmented artificial skin became lighter after treatment with KHG26792. In summary, our findings suggest that KHG26792 is a novel skin whitening agent.