http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Protective effect of Korean Red Ginseng against FK506-induced damage in LLC-PK1 cells
Lee, Dahae,Kang, Ki Sung,Yu, Jae Sik,Woo, Jung-Yoon,Hwang, Gwi Seo,Eom, Dae-Woon,Baek, Seung-Hoon,Lee, Hye Lim,Kim, Ki Hyun,Yamabe, Noriko The Korean Society of Ginseng 2017 Journal of Ginseng Research Vol.41 No.3
Background: Compound FK506 is an immunosuppressant agent that is frequently used to prevent rejection of solid organs upon transplant. However, nephrotoxicity due to apoptosis and inflammatory response mediated by FK506 limit its usefulness. In this study, the protective effect of Korean Red Ginseng (KRG) against FK506-induced damage in LLC-PK1 pig kidney epithelial cells was investigated. Methods: LLC-PK1 cells were exposed to FK506 with KRG and cell viability was measured. Western blotting and RT-PCR analyses evaluated protein expression of MAPKs, caspase-3, and KIM-1. TLR-4 gene expression was assessed. Caspase-3 activities were also determined. The number of apoptotic cells was measured using an image-based cytometric assay. Results: The reduction in LLC-PK1 cell viability by $60{\mu}M$ FK506 was recovered by KRG cotreatment in a dose-dependent manner. The phosphorylation of p38, p44/42 MAPKs (ERK), KIM-1, cleaved caspase-3, and TLR-4 mRNA expression was increased markedly in LLC-PK1 cells treated with $60{\mu}M$ FK506. However, with the exception of p-ERK, elevated levels of p-p38, KIM-1, cleaved caspase-3, and TLR-4 mRNA expression were significantly decreased after cotreatment with KRG. Activity level of caspase-3 was also attenuated by KRG cotreatment. Moreover, image-based cytometric assay showed that apoptotic cell death was increased by $60{\mu}M$ FK506 treatment, whereas it was decreased after cotreatment with KRG. Conclusion: Taken together, these results suggest that the molecular mechanism of KRG in the FK506-induced nephrotoxicity may lead to the development of an adjuvant for the inhibition of adverse effect FK506 in the kidney.
Protective effect of Korean Red Ginseng against FK506-induced damage in LLC-PK1 cells
Dahae Lee,Ki Sung Kang,Jae Sik Yu,Jung-Yoon Woo,Gwi Seo Hwang,Dae-Woon Eom,Seung-Hoon Baek,Hye Lim Lee,Ki Hyun Kim,Noriko Yamabe 고려인삼학회 2017 Journal of Ginseng Research Vol.41 No.3
Background: Compound FK506 is an immunosuppressant agent that is frequently used to prevent rejection of solid organs upon transplant. However, nephrotoxicity due to apoptosis and inflammatory response mediated by FK506 limit its usefulness. In this study, the protective effect of Korean Red Ginseng (KRG) against FK506-induced damage in LLC-PK1 pig kidney epithelial cells was investigated. Methods: LLC-PK1 cells were exposed to FK506 with KRG and cell viability was measured. Western blotting and RT-PCR analyses evaluated protein expression of MAPKs, caspase-3, and KIM-1. TLR-4 gene expression was assessed. Caspase-3 activities were also determined. The number of apoptotic cells was measured using an image-based cytometric assay. Results: The reduction in LLC-PK1 cell viability by 60mM FK506 was recovered by KRG cotreatment in a dose-dependent manner. The phosphorylation of p38, p44/42 MAPKs (ERK), KIM-1, cleaved caspase-3, and TLR-4 mRNA expression was increased markedly in LLC-PK1 cells treated with 60mM FK506. However, with the exception of p-ERK, elevated levels of p-p38, KIM-1, cleaved caspase-3, and TLR-4 mRNA expression were significantly decreased after cotreatment with KRG. Activity level of caspase-3 was also attenuated by KRG cotreatment. Moreover, image-based cytometric assay showed that apoptotic cell death was increased by 60mM FK506 treatment, whereas it was decreased after cotreatment with KRG. Conclusion: Taken together, these results suggest that the molecular mechanism of KRG in the FK506-induced nephrotoxicity may lead to the development of an adjuvant for the inhibition of adverse effect FK506 in the kidney.
Dahae Lee,Ki Sung Kang,Sanghyun Lee,Eun Ju Cho,Hyun Young Kim 한국식품영양과학회 2016 Preventive Nutrition and Food Science Vol.21 No.4
Reactive oxygen species are tumorigenic by their ability to increase cell proliferation, survival, and cellular migration. The purpose of the present study was to compare the antioxidant activity and cytotoxic effects of 3 berry extracts (strawberry, Korean raspberry, and mulberry) in A2780 human ovarian carcinoma cells. Except for raspberry, the ethyl acetate or methylene chloride fractions of berries containing phenolic compounds exerted dose dependent free radical scavenging activities. In the raspberry fractions, the hexane fraction also exhibited potent antioxidant activity. The cytotoxic effects of berries extracts in A2780 human ovarian carcinoma cells were measured using the 3-(4,5-dimethylthiazol- 2-yl)-2,5-diphenyltetrazolium bromide assay. Surprisingly, co-treatment with n-butanol (BuOH) fractions of berries showed stronger cytotoxic effects compared to the other fractions. These findings suggest that potent anticancer molecules are found in the BuOH fractions of berries that have stronger cytotoxic activity than antioxidants.
MTA1 is a novel regulator of autophagy that induces tamoxifen resistance in breast cancer cells
Lee, Min-Ho,Koh, Dahae,Na, Hyelin,Ka, Na-Lee,Kim, Seungsu,Kim, Hyeon-Ji,Hong, Sungyoul,Shin, Young Kee,Seong, Je Kyung,Lee, Mi-Ock TaylorFrancis 2018 AUTOPHAGY Vol.14 No.5
<P><B>ABSTRACT</B></P><P>Tamoxifen is commonly used to treat patients with ESR/ER-positive breast cancer, but its therapeutic benefit is limited by the development of resistance. Recently, alterations in macroautophagy/autophagy function were demonstrated to be a potential mechanism for tamoxifen resistance. Although MTA1 (metastasis-associated 1) has been implicated in breast tumorigenesis and metastasis, its role in endocrine resistance has not been studied. Here, we report that the level of MTA1 expression was upregulated in the tamoxifen resistant breast cancer cell lines MCF7/TAMR and T47D/TR, and knockdown of MTA1 sensitized the cells to 4-hydroxytamoxifen (4OHT). Moreover, knockdown of MTA1 significantly decreased the enhanced autophagy flux in the tamoxifen resistant cell lines. To confirm the role of MTA1 in the development of tamoxifen resistance, we established a cell line, MCF7/MTA1, which stably expressed MTA1. Compared with parental MCF7, MCF7/MTA1 cells were more resistant to 4OHT-induced growth inhibition in vitro and in vivo, and showed increased autophagy flux and higher numbers of autophagosomes. Knockdown of ATG7 or cotreatment with hydroxychloroquine, an autophagy inhibitor, restored sensitivity to 4OHT in both the MCF7/MTA1 and tamoxifen resistant cells. In addition, AMP-activated protein kinase (AMPK) was activated, probably because of an increased AMP:ATP ratio and decreased expression of mitochondrial electron transport complex components. Finally, publicly available breast cancer patient datasets indicate that MTA1 levels correlate with poor prognosis and development of recurrence in patients with breast cancer treated with tamoxifen. Overall, our findings demonstrated that MTA1 induces AMPK activation and subsequent autophagy that could contribute to tamoxifen resistance in breast cancer.</P>
Lee, Dahae,Lee, Dong-Soo,Jung, Kiwon,Hwang, Gwi Seo,Lee, Hye Lim,Yamabe, Noriko,Lee, Hae-Jeong,Eom, Dae-Woon,Kim, Ki Hyun,Kang, Ki Sung The Korean Society of Ginseng 2018 Journal of Ginseng Research Vol.42 No.1
Background: The aim of the present study was to evaluate the potential protective effects of six ginsenosides (Rb1, Rb2, Rc, Rd, Rg1, and Rg3) isolated from Panax ginseng against tacrolimus (FK506)-induced apoptosis in renal proximal tubular LLC-PK1 cells. Methods: LLC-PK1 cells were treated with FK506 and ginsenosides, and cell viability was measured. Protein expressions of mitogen-activated protein kinases, caspase-3, and kidney injury molecule-1 (KIM-1) were evaluated by Western blotting analyses. The number of apoptotic cells was measured using an image-based cytometric assay. Results: Reduction in cell viability by $60{\mu}M$ FK506 was ameliorated significantly by cotreatment with ginsenosides Rg1 and Rb1. The phosphorylation of p38, extracellular signal-regulated kinases, and KIM-1, and cleavage of caspase-3, increased markedly in LLC-PK1 cells treated with FK506 and significantly decreased after cotreatment with ginsenoside Rb1. The number of apoptotic cells decreased by 6.0% after cotreatment with ginsenoside Rb1 ($10{\mu}M$ and $50{\mu}M$). Conclusion: The antiapoptotic effects of ginsenoside Rb1 on FK506-induced apoptosis were mediated by the inhibition of mitogen-activated protein kinases and caspase activation.
Lee, Dahae,Yu, Jae Sik,Lee, Seoung Rak,Hwang, Gwi Seo,Kang, Ki Sung,Park, Jae Gyu,Kim, Hyun Young,Kim, Ki Hyun,Yamabe, Noriko MDPI AG 2018 INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES Vol.19 No.4
<P>Mulberry, the fruit of white mulberry tree (<I>Morus alba</I> L., Moraceae), is commonly used in traditional Chinese medicines as a sedative, tonic, laxative, and emetic. In our continuing research of the bioactive metabolites from mulberry, chemical analysis of the fruits led to the isolation of five compounds, <B>1</B>–<B>5</B>. The compounds were identified as butyl pyroglutamate (<B>1</B>), quercetin 3-<I>O</I>-β-<SMALL>D</SMALL>-glucoside (<B>2</B>), kaempferol 3-<I>O</I>-β-<SMALL>D</SMALL>-rutinoside (<B>3</B>), rutin (<B>4</B>), and 2-phenylethyl <SMALL>D</SMALL>-rutinoside (<B>5</B>) by spectroscopic data analysis, comparing their nuclear magnetic resonance (NMR) data with those in published literature, and liquid chromatography–mass spectrometry analysis. The isolated compounds <B>1</B>–<B>5</B> were evaluated for their effects on anticancer drug-induced side effects by cell-based assays. Compound <B>1</B> exerted the highest protective effect against cisplatin-induced kidney cell damage. This effect was found to be mediated through the attenuation of phosphorylation of c-Jun N-terminal kinase, extracellular signal-regulated kinase, p38, mitogen-activated protein kinase, and caspase-3 in cisplatin-induced kidney cell damage.</P>
Lee, Seulah,Lee, Dahae,Baek, Jiwon,Jung, Eun Bee,Baek, Ji Yun,Lee, Il Kyun,Jang, Tae Su,Kang, Ki Sung,Kim, Ki Hyun TaylorFrancis 2017 PHARMACEUTICAL BIOLOGY Vol.55 No.1
<P><B>Abstract</B></P><P><B>Context:</B> Antiacetylcholinesterase (AChE) drugs have been a main therapeutic treatment for Alzheimer’s disease because increased AChE levels play a key role in reducing neurotransmission.</P><P><B>Objectives:</B> Extracts from 35 Korean plants were selected and screened for antioxidant and anti-cholinesterase activity to explore new sources derived from Korean natural resources that could be used as AD therapeutic agents.</P><P><B>Materials and methods:</B> The antioxidant effect of extracts from 35 selected Korean plants was determined using two most common free radical scavenging assays using 1,1-diphenyl-2-picrylhydrazyl (DPPH) and 2,2′-azino-bis-3-ethylbenzthiazoline-6-sulphonic acid (ABTS). Additionally, the effect of extracts, identified as antioxidants, on acetylcholinesterase inhibition was assessed by an acetylcholinesterase assay kit.</P><P><B>Results:</B> Out of 36 extracts of 35 plants tested, <I>Oenothera biennis</I> L. (9.09 μg/mL), <I>Saururus chinensis</I> (Lour.) Baill. (9.52 μg/mL) and <I>Betula platyphylla</I> var. <I>japonica</I> (9.85 μg/mL) showed strong DPPH scavenging activity. Twelve other extracts also exerted moderate free radical scavenging activities with IC<SUB>50</SUB> values ranging from 10 to 50 μg/mL. Antioxidant capacity detected by ABTS assay was only significant in <I>O. biennis</I> (23.40 μg/mL), while the other extracts were weak or unable to reduce the production of ABTS. Based on the antioxidant activities of these plant extracts, 19 extracts with IC<SUB>50</SUB> values less than 100 μg/mL in DPPH assay were selected for further AChE inhibition assay. Among the extracts tested, the IC<SUB>50</SUB> value for <I>Prunella vulgaris</I> var. <I>lilacina</I> NAKAI (18.83 μg/mL) in AChE inhibitory activity was the lowest, followed by <I>O. biennis</I> (20.09 μg/mL) and <I>Pharbitis nil</I> Chosy (22.79 μg/mL).</P><P><B>Conclusions:</B> Considering complex multifactorial etiology of AD, the extracts of <I>P. vulgaris</I> var. <I>lilacina</I> (aerial part), <I>O. biennis</I> (seed) and <I>P. nil</I> (seed) may be safe and ideal candidates for future AD modifying therapies.</P>