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계지 열수추출물의 대장암세포에서의 활성산소 의존 세포사멸 유도활성
Gwang Hun Park,Yurry Um,Yunmi Park,Chungryul Jung,Kwon Seok Jeon,Jin Boo Jeong 한국약용작물학회 2017 한국약용작물학술대회 발표집 Vol.2017 No.05
Background : The young stem of Cinnamomum cassia (YSC) as traditional Chinese medicines has been reported to show a variety of pharmacological properties such as anti-allergy, insecticidal, antimicrobial, antiulcer, anti-inflammatory, immune-suppressive, and neuronal death prevention, tyrosinase inhibition and anticancer, antioxidant and free radical scavenging, as well as antidiabetic and aldose reductase inhibition activities. In this study, we elucidated apoptotic effect and potential molecular mechanism of hot water extracts from YSC (YSC-HW) against human colorectal cancer cells. Methods and Results : YSC-HW treatment increased ROS level and induced ROS-dependent DNA damage in human colorectal cancer cells. ROS generation mediated by YSC-HW induced DNA induced apoptosis and reduction of cell viability in human colorectal cancer cells. YSC-HW ROS-dependently induced NF-kB activation through p65 nuclear translocation via IkB-α degradation, which exerted the induction of apoptosis. In addition, YSC-HW activated ATF3 expression dependent on ROS, which resulted in apoptosis. Conclusion : Our results suggest that YSC-HW may induce apoptosis through ROS-activation of NF-kB and ATF3 in human colorectal cancer cells. From these findings, YSC-HW has potential to be a candidate for the development of chemoprevention or therapeutic agents for human colorectal cancer.
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Park, Gwang Hun,Hong, Se Chul,Jeong, Jin Boo The Plant Resources Society of Korea 2016 한국자원식물학회지 Vol.29 No.3
The seed of safflower (Carthamus tinctorius L) has been reported to suppress human cancer cell proliferation. However, the mechanisms by which safflower seed inhibits cancer cell proliferation have remained nuclear. In this study, the inhibitory effect of the safflower seed (SS) on the proliferation of human colorectal cancer cells and the potential mechanism of action were examined. SS inhibited markedly the proliferation of human colorectal cancer cells (HCT116, SW480, LoVo and HT-29). In addition, SS suppressed the proliferation of human breast cancer cells (MDA-MB-231 and MCF-7). SS treatment decreased cyclin D1 protein level in human colorectal cancer cells and breast cancer cells. But, SS-mediated downregulated mRNA level of cyclin D1 was not observed. Inhibition of proteasomal degradation by MG132 attenuated cyclin D1 downregulation by SS and the half-life of cyclin D1 was decreased in SS-treated cells. In addition, SS increased cyclin D1 phosphorylation at threonine-286 and a point mutation of threonine-286 to alanine attenuated SS-mediated cyclin D1 degradation. Inhibition of ERK1/2 by PD98059 suppressed cyclin D1 phosphorylation and downregulation of cyclin D1 by SS. In conclusion, SS has anti-proliferative activity by inducing cyclin D1 proteasomal degradation through ERK1/2-dependent threonine-286 phosphorylation of cyclin D1. These findings suggest that possibly its extract could be used for treating colorectal cancer.
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Park, Gwang Hun,Song, Hun Min,Jeong, Jin Boo The Korean Society of Applied Pharmacology 2017 Biomolecules & Therapeutics(구 응용약물학회지) Vol.25 No.3
Kahweol as a coffee-specific diterpene has been reported to induce apoptosis in human cancer cells. Although some molecular targets for kahweol-mediated apoptosis have been elucidated, the further mechanism for apoptotic effect of kahweol is not known. Activating transcription factor 3 (ATF3) has been reported to be associated with apoptosis in colorectal cancer. The present study was performed to investigate the molecular mechanism by which kahweol stimulates ATF3 expression and apoptosis in human colorectal cancer cells. Kahweol increased apoptosis in human colorectal cancer cells. It also increased ATF3 expression through the transcriptional activity. The responsible cis-element for ATF3 transcriptional activation by kahweol was CREB located between -147 to -85 of ATF3 promoter. ATF3 overexpression increased kahweol-mediated cleaved PARP, while ATF3 knockdown attenuated the cleavage of PARP by kahweol. Inhibition of ERK1/2 and $GSK3{\beta}$ blocked kahweol-mediated ATF3 expression. The results suggest that kahweol induces apoptosis through ATF3-mediated pathway in human colorectal cancer cells.
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Wood-cultivated ginseng exerts anti-inflammatory effect in LPS-stimulated RAW264.7 cells
Park, Su Bin,Park, Gwang Hun,Um, Yurry,Kim, Ha Na,Song, Hun Min,Kim, Nahyun,Kim, Hyun-Seok,Jeong, Jin Boo Elsevier 2018 INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES Vol.116 No.-
<P><B>Abstract</B></P> <P>Ginseng (<I>Panax ginseng</I>) has been reported to exert an anti-inflammatory activity in a variety of inflammatory condition. However, inflammation-regulatory activity of wood-cultivated ginseng has not been thoroughly evaluated. In this study, we evaluated the anti-inflammatory effect of wood-cultivated ginseng (WCG) and elucidated the potential mechanisms in LPS-stimulated RAW264.7 cells. WCG-O dose-dependently suppressed NO and PGE<SUB>2</SUB> production in LPS-stimulated RAW264.7 cells. In addition, WCG-O attenuated LPS-mediated overexpression of iNOS and COX-2. In addition, WCG-O blocked the expression of TNF-α and IL-1β. WCG-O inhibited the activation of IκK-α/β, the phosphorylation of IκB-α, and degradation of IκB-α, which results in the inhibition of p65 nuclear accumulation and NF-κB activation. In addition, WCG-O suppressed the activation of ERK1/2, p38 and JNK, which results in the inhibition of ATF2 nuclear accumulation. These results indicate that WCG-O may exert anti-inflammatory activity by inhibiting NF-κB and MAPK signaling. From these findings, WCG-O has potential to be a candidate for the development of chemopreventive or therapeutic agents for the inflammatory diseases.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Wood-cultivated ginseng suppresses NO and PGE<SUB>2</SUB> production through iNOS and COX-2 expression </LI> <LI> Wood-cultivated ginseng inhibits the expression of the inflammatory cytokines such as TNF-α and IL-1β </LI> <LI> Wood-cultivated ginseng inhibits NF-κB activation by blocking IκB-α degradation and subsequent p65 nuclear translocation </LI> <LI> Wood-cultivated ginseng inhibits ATF2 nuclear accumulation through suppressing MAPK activation </LI> </UL> </P>
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Park, Su Bin,Park, Gwang Hun,Kim, Ha Na,Son, Ho-Jun,Song, Hun Min,Kim, Hyun-Seok,Jeong, Hyung Jin,Jeong, Jin Boo Elsevier 2018 BIOMEDICINE AND PHARMACOTHERAPY Vol.104 No.-
<P><B>Abstract</B></P> <P>Mistletoe has been used as the herbal medicine to treat hypertension, diabetes mellitus, inflammation, arthritis and viral infection. In this study, we evaluated the anti-inflammatory effect of extracts of branch from <I>Taxillus yadoriki</I> being parasitic in <I>Neolitsea sericea</I> (TY-NS-B) using <I>in vitro</I> model. TY-NS-B significantly inhibited LPS-induced secretion of NO and PGE<SUB>2</SUB> in RAW264.7 cells. TY-NS-B was also observed to inhibit LPS-mediated iNOS COX-2 expression. In addition, TY-NS-B attenuated production of inflammatory cytokines such as TNF-α and IL-1β induced by LPS. TY-NS-B blocked LPS-mediated inhibitor of IκB-α, and inhibited p65 translocation to the nucleus and NF-κB activation. Furthermore, TY-NS-B reduced the phosphorylation of MAPKs such as p38 and JNK, but not ERK1/2. In addition, TY-NS-B increased ATF3 expression and ATF3 knockdown by ATF3 siRNA attenuated TY-NS-B-mediated inhibition of pro-inflammatory mediator expression. Collectively, our results suggest that TY-NS-B exerts potential anti-inflammatory effects by suppressing NF-κB and MAPK signaling activation, and increasing ATF3 expression. These findings indicate that TY-NS-B could be further developed as an anti-inflammatory drug.</P> <P><B>Highlights</B></P> <P> <UL> <LI> TY-NS-B blocks NO and PGE2 production by inhibiting iNOS and COX-2 expression. </LI> <LI> TY-NS-B attenuates TNF-α and IL-1β expression. </LI> <LI> TY-NS-B inhibits NF-κB activating by inhibiting IκB-α degradation and subsequent p65 nucleus translocation. </LI> <LI> TY-NS-B inhibits p38 and JNK activation. </LI> <LI> TY-NS-B activates ATF3 expression. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>
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( Gwang Hun Park ),( Hun Min Song ),( Jin Boo Jeong ) 한국응용약물학회 2017 Biomolecules & Therapeutics(구 응용약물학회지) Vol.25 No.3
Kahweol as a coffee-specific diterpene has been reported to induce apoptosis in human cancer cells. Although some molecular targets for kahweol-mediated apoptosis have been elucidated, the further mechanism for apoptotic effect of kahweol is not known. Activating transcription factor 3 (ATF3) has been reported to be associated with apoptosis in colorectal cancer. The present study was performed to investigate the molecular mechanism by which kahweol stimulates ATF3 expression and apoptosis in human colorectal cancer cells. Kahweol increased apoptosis in human colorectal cancer cells. It also increased ATF3 expression through the transcriptional activity. The responsible cis-element for ATF3 transcriptional activation by kahweol was CREB located between -147 to -85 of ATF3 promoter. ATF3 overexpression increased kahweol-mediated cleaved PARP, while ATF3 knockdown attenuated the cleavage of PARP by kahweol. Inhibition of ERK1/2 and GSK3β blocked kahweol-mediated ATF3 expression. The results suggest that kahweol induces apoptosis through ATF3-mediated pathway in human colorectal cancer cells.
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Park, Gwang Hun,Park, Jae Ho,Eo, Hyun Ji,Song, Hun Min,Lee, Man Hyo,Lee, Jeong Rak,Jeong, Jin Boo The Plant Resources Society of Korea 2014 한국자원식물학회지 Vol.27 No.3
In this study, we investigated whether A. distichum decreases the production of inflammatory mediators through downregulation of the NF-${\kappa}B$ and ERK pathway. Our data indicated that A. distichum leaf inhibits the overexpression of iNOS in protein and mRNA levels, and subsequently blocked LPS-mediated NO overproduction in RAW264.7 cells. A. distichum leaf inhibited $I{\kappa}B-{\alpha}$ degradation and p65 nuclear translocation, and subsequently suppressed transcriptional activity of NF-${\kappa}B$ in LPS-stimulated RAW264.7 cells. In addition, A. distichum leaf suppressed LPS-induced ERK1/2 activation by decreasing phosphorylation of ERK1/2. These findings suggest that A. distichum leaf shows anti-inflammatory activities through suppressing ERK-mediated NF-${\kappa}B$ activation in mouse macrophage.
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박광헌 ( Park Gwang-hun ) 동아문화재단 2019 文物硏究 Vol.- No.35
현재는 사경을 칭할 때 “종이의 색+필사재료+서명”의 방식으로 표기하는 것이 공식화 되어 있다. 사경 명칭 중 서명 앞의 수식어에 대한 역사적 용례에 대해 살펴보았다. 짙은 청색의 寫經紙를 지칭하는 전통적인 용어는 ‘紺紙’가 아니라 ‘鴉靑紙’가 가장 대표적으로 사용되었으며, 색상의 표현은 ‘藍色’이 흔히 사용되었다. ‘橡紙’는 1980년도 즈음에 새롭게 정립된 용어로 판단되며, 그 이전에는 ‘茶紙’, ‘褐紙’, ‘茶褐紙’, ‘紅紙’ 등으로 다양하게 사용되었다. ‘橡紙’는 실제 도토리나무 수액이나 도토리 열매를 통해 염색하였는지 기록이나 과학적 검증 없이 사용되는 문제점이 있다. ‘紫紙’의 경우는 자색의 寫經紙를 뜻하나 ‘橡紙’의 변색으로 보는 시각도 있어 ‘橡紙’와 함께 과학적인 비교 분석이 필요하다. 필사의 재료를 뜻하는 ‘金泥’와 ‘銀泥’는 현재 통용되고 있지만 전통적으로 사경을 표현할 때는 ‘金字’와 ‘銀字’로 표현하였음을 알 수 있다. Currently, it is official to write the name of the Buddhist Manuscript of “paper's color + type of ink + book name.” This study analyzes on the words that are modelled in front of the Buddhist Manuscript’s name The traditional term for paper of the Buddhist Manuscript was used most commonly ‘鴉靑紙(Achungji)’, not ‘紺紙(Gamji)’ and the expression of colors was ‘藍色(Gamsaek)’. ‘橡紙(Sangji)’ is a newly coined term around 1980. And Various terms were used before. The problem with the term "橡紙(Sangji)" is that it is not known whether it is actually dyed with acorn trees. There is no record or scientific verification associated with such dyeing. ‘紫紙(Jaji)’ means that the color of purple paper of Buddhist Manuscript, but there are some views that ‘橡紙(Sangji)’ is discolored. So ‘紫紙(Jaji)’ and ‘橡紙(Sangji)’ need scientific comparative analysis. ‘金泥(Geumni)’ and ‘銀泥(eunni)’ are now commonly used to mean the kind of ink written in the Buddhist Manuscript, but the traditional terms are ‘金字(Geumja)’ and ‘金字(eumja)’.
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