http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Piao, Mei Jing,Kim, Ki Cheon,Zheng, Jian,Yao, Cheng Wen,Cha, Ji Won,Boo, Sun Jin,Yoon, Weon Jong,Kang, Hee Kyoung,Yoo, Eun Sook,Koh, Young Sang,Ko, Mi Hee,Lee, Nam Ho,Hyun, Jin Won Informa Healthcare USA, Inc. 2014 PHARMACEUTICAL BIOLOGY Vol.52 No.9
<P><I>Context</I>: Our previous work demonstrated that an ethyl acetate extract derived from <I>Sargassum muticum</I> (Yendo) Fenshol (SME) protected human HaCaT keratinocytes against ultraviolet B (UVB)-induced oxidative stress by increasing antioxidant activity in the cells, thereby inhibiting apoptosis.</P><P><I>Objective</I>: The aim of the current study was to further elucidate the anti-apoptotic mechanism of SME against UVB-induced cell damage.</P><P><I>Materials and methods</I>: The expression levels of several apoptotic-associated and mitogen-activated kinase (MAPK) signaling proteins were determined by western blot analysis of UVB-irradiated HaCaT cells with or without prior SME treatment. In addition, the loss of mitochondrial membrane potential (Δ<I>ψ</I><SUB>m</SUB>) was detected using flow cytometry or confocal microscopy and the mitochondria membrane-permeate dye, JC-1. Apoptosis was assessed by quantifying DNA fragmentation and apoptotic body formation. Furthermore, cell viability was evaluated using the MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay.</P><P><I>Results</I>: SME absorbed electromagnetic radiation in the UVB range (280-320 nm) of the UV/visible light spectrum. SME also increased Bcl-2 and Mcl-1 expression in UVB-irradiated cells and decreased the Bax expression. Moreover, SME inhibited the UVB-induced disruption of mitochondrial membrane potential and prevented UVB-mediated increases in activated caspase-9 and caspase-3 (an apoptotic initiator and executor, respectively) levels. Notably, treatment with a pan-caspase inhibitor enhanced the anti-apoptotic effects of SME in UVB-irradiated cells. Finally, SME reduced the UVB-mediated phosphorylation of p38 MAPK and JNK, and prevented the UVB-mediated dephosphorylation of Erk1/2 and Akt.</P><P><I>Discussion and conclusion</I>: The present results indicate that SME safeguards HaCaT keratinocytes from UVB-mediated apoptosis by inhibiting a caspase-dependent signaling pathway.</P>
Phloroglucinol inhibits ultraviolet B radiation-induced oxidative stress in the mouse skin
Piao, Mei Jing,Ahn, Mee Jung,Kang, Kyoung Ah,Kim, Ki Cheon,Zheng, Jian,Yao, Cheng Wen,Cha, Ji Won,Hyun, Chang Lim,Kang, Hee Kyoung,Lee, Nam Ho,Hyun, Jin Won Informa Healthcare 2014 International journal of radiation biology Vol.90 No.10
<P><I>Purpose</I>: Previously we demonstrated that phloroglucinol (1,3,5-trihydroxybenzene) protected human HaCaT keratinocytes against ultraviolet B (UVB, 280-320 nm)-induced oxidative stress <I>in vitro</I> by scavenging intracellular reactive oxygen species (ROS). The current study investigated whether phloroglucinol could similarly protect the mouse skin against UVB-induced oxidative tissue damage <I>in vivo</I>.</P><P><I>Materials and methods</I>: Male 7-week-old Balb/c mice were divided into the following untreated normal control, phloroglucinol only-treated, vehicle plus UVB (30 or 60 mJ/cm<SUP>2</SUP>)-exposed, and phloroglucinol (10 or 50 mg/ml) plus UVB (30 or 60 mJ/cm<SUP>2</SUP>)-treated groups. Following UVB exposure, phloroglucinol or phosphate buffered saline vehicle was applied to the dorsal skin of each mouse daily for 3 days. Studies were conducted at 24 h after the last of the UVB exposures. Histopathological analyses of dorsal skin lesions were performed on all mice. In addition, the levels of UVB-provoked injury to cellular components, including DNA, proteins, and lipids were detected by levels of 8-oxoguanine (8-oxoG), protein carbonyls, and 8-isoprostane. Apoptosis were assessed by using western blot for B-cell lymphoma-2-associated X protein (Bax) and activated caspase-3 expression, by using immunohistochemistry.</P><P><I>Results</I>: UVB radiation increased the thickness of the epidermis and the dermis, and also stimulated the accumulation of mast cells in the irradiated skin. However, treatment with phloroglucinol significantly decreased all of these parameters. Furthermore, phloroglucinol decreased UVB-provoked injury to cellular components, including DNA, proteins, and lipids; down-regulated the expression of phospho-histone H2A.X in the injured skin; and reduced the UVB-generated levels of 8-oxoG, protein carbonyls, and 8-isoprostane, which are all markers of oxidative stress. In addition, phloroglucinol attenuated the UVB-induced expression of the pro-apoptotic proteins, Bax protein, and activated caspase-3.</P><P><I>Conclusion</I>: These results suggest that phloroglucinol safeguards the mouse skin against UVB-induced oxidative stress and apoptosis.</P>
Ju-Ya Hsiao,Chun-Yao Chen,Mei-Jun Yang,Han-Chen Ho 한국미생물학회 2013 The journal of microbiology Vol.51 No.3
Caenorhabditis elegans has been used for studying hostpathogen interactions since long, and many virulence genes of pathogens have been successfully identified. In several studies, fluorescent pathogens were fed to C. elegans and fluorescence observed in the gut was considered an indicator for bacterial colonization. However, the grinder in the pharynx of these nematodes supposedly crushes the bacterial cells, and the ground material is delivered to the intestine for nutrient absorption. Therefore, it remains unclear whether intact bacteria pass through the grinder and colonize in the intestine. Here we investigated whether the appearance of fluorescence is indicative of intact bacteria in the gut using both fluorescence microscopy and transmission electron microscopy. In wild-type N2 C. elegans, Escherichia coli DH5α, and Vibrio vulnificus 93U204, both of which express the green fluorescence protein, were found intact only proximal to the grinder, while crushed bacterial debris was found in the post-pharyngeal lumen. Nevertheless, the fluorescence was evident throughout the lumen of worm intestines irrespective of whether the bacteria were intact or not. We further investigated the interaction of the bacteria with C. elegans phm-2 mutant, which has a dysfunctional grinder. Both strains of bacteria were found to be intact and accumulated in the pharynx and intestine owing to the defective grinder. The fluorescence intensity of intact bacteria in phm-2 worms was indistinguishable from that of crushed bacterial debris in N2 worms. Therefore, appearance of fluorescence in the C. elegans intestine should not be directly interpreted as successful bacterial colonization in the intestine.
( Ki Cheon Kim ),( Mei Jing Piao ),( Jian Zheng ),( Cheng Wen Yao ),( Ji Won Cha ),( Madduma Hewage Susara Ruwan Kumara ),( Xia Han ),( Hee Kyoung Kang ),( Nam Ho Lee ),( Jin Won Hyun ) 한국응용약물학회 2014 Biomolecules & Therapeutics(구 응용약물학회지) Vol.22 No.4
Fucodiphlorethol G (6`-[2,4-dihydroxy-6-(2,4,6-trihydroxyphenoxy)phenoxy]biphenyl-2,2`,4,4`,6-pentol) is a compound purifi ed from Ecklonia cava, a brown alga that is widely distributed offshore of Jeju Island. This study investigated the protective effects of fucodiphlorethol G against oxidative damage-mediated apoptosis induced by ultraviolet B (UVB) irradiation. Fucodiphlorethol G attenuated the generation of 2, 2-diphenyl-1-picrylhydrazyl radicals and intracellular reactive oxygen species in response to UVB irradiation. Fucodiphlorethol G suppressed the inhibition of human keratinocyte growth by UVB irradiation. Additionally, the wavelength of light absorbed by fucodiphlorethol G was close to the UVB spectrum. Fucodiphlorethol G reduced UVB radiation-induced 8-isoprostane generation and DNA fragmentation in human keratinocytes. Moreover, fucodiphlorethol G reduced UVB radiationinduced loss of mitochondrial membrane potential, generation of apoptotic cells, and active caspase-9 expression. Taken together, fucodiphlorethol G protected human keratinocytes against UVB radiation-induced cell damage and apoptosis by absorbing UVB radiation and scavenging reactive oxygen species.
Dictyopteris undulata Extract Induces Apoptosis in Human Colon Cancer Cells
Kim, Areum Daseul,Kang, Kyoung Ah,Piao, Jing Mei,Kim, Ki Cheon,Zheng, Jian,Yao, Cheng Wen,Cha, Ji Won,Hyun, Chang Lim,Boo, Sun Jin,Lee, Nam Ho,Na, Soo Young,Hyun, Jin Won 한국생물공학회 2014 Biotechnology and Bioprocess Engineering Vol.19 No.3
The present study investigated the cytotoxic and apoptotic effects of an ethanol extract derived from the marine brown alga Dictyopteris undulata against human colon adenocarcinoma cells. The Dictyopteris undulata extract (DUE) showed cytotoxic activity against SW480 cells in a dose-dependent manner, with 50% inhibition of cell viability at a concentration of $40{\mu}g/mL$. DUE also induced programmed cell death in SW480 cells, as evidenced by apoptotic body formation, DNA fragmentation, an increase in the population of apoptotic sub-$G_1$ phase cells, and mitochondrial membrane depolarization. Moreover, DUE significantly modulated the expression of apoptosis-associated proteins, resulting in a decrease in B cell lymphoma-2 expression and an increase in Bcl-2-associated X protein expression, as well as the activation of caspase-9 and caspase-3. Furthermore, DUE showed apoptotic cell death in two other colon cancer cell lines, SNU407 and HT29. These observations suggest that DUE may prove useful as a therapeutic agent for the attenuation of colon cancer.