http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Isolation of Anticancer Compounds from Peucedanum japonicum Thunb. Roots
Jun, Neung Jae,Kim, Seong-Cheol,Song, Eun-Young,Jang, Ki Chang,Lee, Dong Sun,Cho, Somi K. The Plant Resources Society of Korea 2014 한국자원식물학회지 Vol.27 No.3
This study was conducted to isolate a compound with anticancer properties from the roots of Peucedanum japonicum Thunb. (Umbelliferae), and to evaluate the efficacy of that compound's anticancer activity. The $CHCl_3$ layer was purified via repeated column chromatography and recrystallization. The two compounds isolated from $CHCl_3$ layer were identified via NMR spectroscopic analysis as (10E) 1,10-heptadecadiene-4,6-diyne-3,8,9-triol (Comp. I) and anomalin (Comp. II). (10E) 1,10-heptadecadiene-4,6-diyne-3,8,9-triol was the first report from the roots of P. japonicum. MTT assays were conducted to evaluate the in vitro cytotoxic activities of Compounds I and II against the following human cancer cell lines: HeLa, HepG2, SNU-16, and AGS. Comp. I evidenced the most profound cytotoxic activity against HepG2 cells ($IC_{50}=6.04{\mu}g/mL$), and Comp. II exhibited the most profound cytotoxic activity against SNU-16 cells ($IC_{50}=18.24{\mu}g/mL$) among the human cancer cell lines tested in this study. However, no significant cell death was observed in the CCD-25Lu human normal lung fibroblast cells. Quantitative analysis using UPLC (Ultra Performance Liquid Chromatography) showed that the roots of P. japonicum contained 0.015 (Comp. I) and 1.69 mg/g (Comp. II) of these compounds.
Jun, Neung-Jae,Jang, Ki-Chang,Kim, Seong-Cheol,Moon, Doo-Young,Seong, Ki-Cheol,Kang, Kyung-Hee,Tandang, Leoncia,Kim, Phil-Hoon,Cho, So-Mi K.,Park, Ki-Hun The Korean Society for Applied Biological Chemistr 2007 Journal of Applied Biological Chemistry (J. Appl. Vol.50 No.4
The contents of total phenol and total flavonoid of artichoke (Cynara scolymus L.) were measured. The antioxidant activity of the artichoke was evaluated based on its potential as a scavenging the ABTS radical. These results showed the antioxidant activity of artichoke has a close relationship with the total flavonoid content. The compound showing antioxidant activity was isolated from the artichoke by repeated column chromatography and recrystallization. Based on the spectrometric studies, the compound was identified as 1,3-dicaffeoylquinic acid, known as cynarin. The content of cynarin from heads and leafs of the artichoke determined by $C_{18}$ reversed phase HPLC (high-performance liquid chromatography) coupled with photodiode array detector was 10.15 and 0.67 mg/g, respectively. This compound showed potent antioxidant activities against DPPH and ABTS radicals ($EC_{50}$ = 14.09 and 28.85 ${\mu}M$, respectively).
TonEBP Promotes Hepatocellular Carcinoma via Promotion of Inflammation
( Jun Ho Lee ),( Neung Hwa Park ),( Hyun Je Kang ),( Jae Hee Suh ),( Chang Jae Kim ),( Hwan Hee Lee ),( Soo Youn Choi ),( Whaseon Lee-kwon ),( Hyug Moo Kwon ) 대한간학회 2016 춘·추계 학술대회 (KASL) Vol.2016 No.1
Aims: Tonicity-responsive enhancer binding protein (TonEBP) is a key transcription cofactor in pro-inflammatory activation of macrophages. TonEBP is involved in inflammatory diseases such as rheumatoid arthritisand atherosclerosis. Since hepatic inflammation is required for the development of hepatocellular carcinoma (HCC), we asked whether TonEBP played a role in HCC. Methods: We studied liver section and tissue biopsy from patients with HBV-, HCV-, and non-viral-induced HCC, obtained from the University of Ulsan college of Medicine . Levels of protein expression and gene expression was measured by western blot analysis and qRT-PCR. Mice with whole body haplo-deficiency of TonEBP and their wild type littermates (C57BL6 background) were given injection of DEN at 2-week-old age and fed the high fat diet or normal control diet for 30 weeks. Mice of hepatocyte-specific (Albcre +/- or -/- floxed with TonEBP) or myeloid-specific TonEBP deletion(LysM cre +/- or -/- floxed with TonEBP) and their wild type littermates were injected DEN at 8-week-old age for 48 hrs. Results: Here we report that TonEBP haplo-insufficiency is resistant not only to diethylnitrosamine (DEN)-induced HCC but also to DEN/high fat diet induced HCC, through attenuation of COX-2 expression and inflammation. In hepatocytes, TonEBP interacts with transcription factor YY1 and histone acetyltransferase p300. This interaction promotes inflammatory stimuli-induced COX-2 expression. Interestingly, hepatic tumor shows higher expression of TonEBP than non-tumor liver in mice and HCC patients. This regulation is associated with miR-223 which expression is down-regulated upon HCC development. In addition, its expression was significantly associated with poor survival of HCC patients after resection. Conclusions: TonEBP is a novel transcription cofactor in COX-2 regulation through transcription factor YY1. With this mechanism, TonEBP is an independent determinant of HCC and novel target for HCC diagnosis and treatment.
Lee, Jun Ho,Suh, Jae Hee,Choi, Soo Youn,Kang, Hyun Je,Lee, Hwan Hee,Ye, Byeong Jin,Lee, Gap Ryol,Jung, Seok Won,Kim, Chang Jae,Lee-Kwon, Whaseon,Park, Jiyoung,Myung, Kyungjae,Park, Neung Hwa,Kwon, Hyu BMJ Publishing Group 2019 Gut: journal of the British Society of Gastroenter Vol.68 No.2
<P><B>Objectives</B></P><P>Hepatocellular carcinoma (HCC) is a common cancer with high rate of recurrence and mortality. Diverse aetiological agents and wide heterogeneity in individual tumours impede effective and personalised treatment. Tonicity-responsive enhancer-binding protein (TonEBP) is a transcriptional cofactor for the expression of proinflammatory genes. Although inflammation is intimately associated with the pathogenesis of HCC, the role of TonEBP is unknown. We aimed to identify function of TonEBP in HCC.</P><P><B>Design</B></P><P>Tumours with surrounding hepatic tissues were obtained from 296 patients with HCC who received completion resection. TonEBP expression was analysed by quantitative reverse transcription–quantitative real-time PCR (RT-PCR) and immunohfistochemical analyses of tissue microarrays. Mice with TonEBP haplodeficiency, and hepatocyte-specific and myeloid-specific TonEBP deletion were used along with HCC and hepatocyte cell lines.</P><P><B>Results</B></P><P>TonEBP expression is higher in tumours than in adjacent non-tumour tissues in 92.6% of patients with HCC regardless of aetiology associated. The TonEBP expression in tumours and adjacent non-tumour tissues predicts recurrence, metastasis and death in multivariate analyses. TonEBP drives the expression of cyclo-oxygenase-2 (COX-2) by stimulating the promoter. In mouse models of HCC, three common sites of TonEBP action in response to diverse aetiological agents leading to tumourigenesis and tumour growth were found: cell injury and inflammation, induction by oxidative stress and stimulation of the COX-2 promoter.</P><P><B>Conclusions</B></P><P>TonEBP is a key component of the common pathway in tumourigenesis and tumour progression of HCC in response to diverse aetiological insults. TonEBP is involved in multiple steps along the pathway, rendering it an attractive therapeutic target as well as a prognostic biomarker.</P>