HeLa 및 Hep G2 세포의 미세구조에 미치는 Taxol의 영향

김광열,김주영,성언기,이융창 대한해부학회 1995 Anatomy & Cell Biology Vol.28 No.5

Anti-proliferative Effect of Coptis Chinensis Extract in Hep G2 Cells

Kim, Jun-Lae,Oh, Se-Mi,Shin, Jang-Woo,Son, Jin-Young,Cho, Jung-Hyo,Lee, Yeon-Weol,Son, Chang-Gue,Cho, Chong-Kwan,Yoo, Hwa-Seung The Society of Korean Medicine 2006 대한한의학회지 Vol.27 No.4

Objectives : This study is aimed to elucidate anti-hepatoma activity of Coptis Chinensis Extract (CCE) and evaluate its effect on proliferation of human hepatoma Hep G2 cells. Methods : To identify CCE and control the quality, we performed fingerprinting by high-performance thin layer chromatography (HPTLC). To investigate effects of CCE on anti-hepatoma activity, we measured cytotoxicity against Hep G2 cells compared with treatment of paclitaxel and 5-fluorouracil (5-FU). To examine the mechanism of inhibitory effect of CCE on Hep G2 cell proliferation, cell cycle distribution was evaluated using fluorescent activated cell sorter (FACS) Result : CCE showed a significant effect that arrests Hep G2 cells at the G2/M phase of the cell cycle. CCE combined with paclitaxel inhibited synergistically cell growth of Hep G2 cells. Conclusion : CCE may present anticancer effects through inhibition of hepatocellular carcinoma (HCC) cell proliferation via G2/M arrest, and may be a useful anticancer agent for HCC.

인진호가 Hep G2 세포에서 에탄올 매개성 Cytokine 분비에 미치는 영향

심정섭,김일환,김강산,강병기,최수덕,Sim, Jung-Sub,Kim, Il-Hwan,Kim, Gang-San,Kagn, Byung-Ki,Choi, Su-Deock 대한한방내과학회 2001 大韓韓方內科學會誌 Vol.22 No.1

A human hepatoma cell line, Hep G2 cells, is reliable for the study of alcohol-induced hepatotoxicity. The aim of this study is to determine the relationship between TNF-${\alpha}$, IL-$1{\alpha}$ production and EtOH-induced cytotoxicity on Hep G2 cells. The cells were incubated with EtOH in the presence of Artemisia Capillaris Herba(AC) for 24 hours and in the absence of AC for 48 hours. Cytoviability and cytokines release were analyzed by MTT assay and enzyme linked immunosorbent assay (ELISA), respectively. After 24 hours of EtOH exposure, the cytoviability had markedly decreased, and the release of cytokines had increased. The increased amount of cytokines contributed to EtOH-induced cytotoxicity. Anti-TNF-${\alpha}$ and IL-$1{\alpha}$ antibodies almost abolished it. Interestingly, EtOH-induced cytotoxicity and cytokines production were inhibited by AC. Moreover, when AC was used in combination with antibodies, there was a marked inhibition of EtOH-induced cytotoxicity. These results suggest that EtOH-induced cytotoxicity may regulate, by various factors, and AC may prevent the cytotoxicity through partial inhibition of the $TNF-{\alpha}$ and IL-$1{\alpha}$ secretion.

Hep3B 간암세포에서 개똥쑥 추출물에 의한 Cell Cycle Arrest 효과

김은지(Eun Ji Kim),김근태(Guen Tae Kim),김보민(Bo Min Kim),임은경(Eun Gyeong Lim),김상용(Sang Yong Kim),하성호(Sung Ho Ha),김영민(Young Min Kim),유제근(Je-Geun Yoo) 한국생물공학회 2015 KSBB Journal Vol.30 No.4

Cells proliferate via repeating process that growth and division. This process is G1, S, G2 and M four phases consists. Monitoring the progression of the cell cycle is a specific step that to be a continuous process is repeated to adjust the start of the next step. At this time, this process is called a Checkpoint. Currently, there are three known checkpoints that G1-S phase, G2-M phase, and the M phase. In this study, we confirmed that cell cycle arrest effects by ethanol extracts of Artemisia annua Linne (AAE) in Hep3B liver cancer cells. AAE was regulated proteins which involved in cell cycle such as pAkt, pMDM2, p53, p21, pCDK2 (T14/Y15). AAE induced cell cycle arrest in G1 checkpoint through phosphorylation of CDK2. Akt and p53 upstream is inhibited by AAE and p53 activated by non-activated pMDM2, p53 inhibitor. Thereby, activated p53 is transcript to p21 and activated p21 protein is combined with Cyclin E-pCDK2 complex. Therefore, we confirmed that AAE-induced cell cycle arrest was occurred by p21-Cyclin E-pCDK2 complex by inhibition of pAkt signal. Because of this cell cycle can’t pass to S phase from G1 phase.

Asparagus cochinchinensis inhibits the ethanol-induced cytotoxicity in Hep G2 cells

Kim, Jeong-Joong Kyung Hee Oriental Medicine Research Center 2000 International journal of oriental medicine Vol.1 No.1

A human hepatoma cell line, Hep G2 cells are a reliable for the study of alcohol-induced hepatotoxicity. In this study, the author investigated the effect of an aqueous extract of Asparagus $cochinchinensis_{MERRIL}$ (Liliaceae) roots (ACAE) on ethanol (EtOH)-induced cytotoxicity in Hep G2 cells. ACAE dose-dependently inhibited the EtOH-induced tumor necrosis $factor-{\alpha}\;(TNF-{\alpha})$ secretion. ACAE also inhibited the EtOH and $TNF-{\alpha}-induced$ cytotoxicity. Furthermore, the author found that ACAE inhibited the $TNF-{\alpha}-induced$ apoptosis of Hep G2 cells. These results suggest that ACAE may prevent the EtOH-induced cytotoxicity through inhibition of the apoptosis of Hep G2 cells.

Anti-cancer Activity of Osmanthus matsumuranus Extract by Inducing G2/M Arrest and Apoptosis in Human Hepatocellular Carcinoma Hep G2 Cells

Soojung JIn,Hyun-Jin Park,HYUN-JU KWON,Jeong-Hwan Kim,최영현,Byung-Woo Kim 대한암예방학회 2015 Journal of cancer prevention Vol.20 No.4

Background: Osmanthus matsumuranus, a species of Oleaceae, is found in East Asia and Southeast Asia. The bioactivities of O. matsumuranus have not yet been fully understood. Here, we studied on the molecular mechanisms underlying anti-cancer effect of ethanol extract of O. matsumuranus (EEOM). Methods: Inhibitory effect of EEOM on cell growth and proliferation was determined by WST assay in various cancer cells. To investigate the mechanisms of EEOM-mediated cytotoxicity, HepG2 cells were treated with various concentration of EEOM and analyzed the cell cycle arrest and apoptosis induction by flow cytometry, Western blot analysis, 4,6-diamidino-2-phenylindole (DAPI) staining and DNA fragmentation. Results: EEOM showed the cytotoxic activities in a dose-dependent manner in various cancer cell lines but not in normal cells, and HepG2 cells were most susceptible to EEOM-induced cytotoxicity. EEOM induced G2/M arrest in HepG2 cells associated with decreased expression of cyclin-dependent kinase 1 (CDK1), cyclin A and cylcin B, and increased expression of phospho-checkpoint kinase 2, p53 and CDK inhibitor p21. Immunofluorescence staining showed that EEOM-treated HepG2 increased doublet nuclei and condensed actin, resulting in cell rounding. Furthermore, EEOM-mediated apoptosis was determined by Annexin V staining, chromatin condensation and DNA fragmentation. EEOM caused upregulation of FAS and Bax, activation of caspase-3, -8, -9, and fragmentation of poly ADP ribose polymerase. Conclusions: These results suggest that EEOM efficiently inhibits proliferation of HepG2 cells by inducing both G2/M arrest and apoptosis via intrinsic and extrinsic pathways, and EEOM may be used as a cancer chemopreventive agent in the food or nutraceutical industry.

상기생과 봉독이 간암 세포주 Hep G2에 대해 미치는 항암 기전 비교

김승욱,김보람,허경,임성우,Kim, Sung-Uk,Kim, Bo-Ram,Heo, Kyung,Lim, Seong-Woo 대한한방내과학회 2009 大韓韓方內科學會誌 Vol.30 No.4

Background and Objectives : Korean mistletoe lectin (Viscum album coloratum agglutinin, VCA) and bee venom (BV) have been reported to induce apoptosis in various cancer cell lines in vitro and to show antitumor activity against a variety of tumors in animal models. However, the comparative effect of VCA and BV on the anti-cancer effect and mechanisms of action has not been determined. In this study, the effect in a human hepatocellular carcinoma cell line, Hep G2 cells, was examined. Methods : Cytotoxic effects of VCA and BV on Hep G2 cells were determined by 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay in litro. The apoptotic cell death was then confirmed by propidium iodide staining and DNA fragmentation analysis. The mechanisms of action were examined by the expression of anti-apoptotic proteins and activation of mitogen-activated protein kinases. The involvement of kinase was examined in VCA or BV-induced apoptosis by using kinase inhibitors. Results : VCA and BV killed Hep G2 cells in a time and dose-dependent manner. Treatment of Hep G2 cells with VCA activated poly (ADP-ribose) polymerase-1 (PARP-1) known as a marker of apoptosis, and mitogen-activated protein kinases signaling pathways including MAPK/ERK, p38 MAPK and JNK. BV also activated PARP-1, MAPK/ERK. and p38 MAPK but not JNK. The expression level of anti-apoptotic molecule, Bcl-X, was decreased by VCA treatment but not by BV. Finally, the phosphorylation level of ERM proteins involved in the cytoskeleton homeostasis was decreased by both stimuli. VCA-induced apoptosis was partially inhibited by in the presence of JNK and p38 inhibitor, but BV only by p38 inhibitor. Conclusions : VCA-induced apoptosis is dependent on the activation of p38 and JNK. while BV-induced apoptosis is mediated by p38 activation in Hep G2 cells.

Hep G2 세포에서 간염제1탕의 에탄올에 의한 세포독성 억제효과

박용권,김강산,강병기,나기웅,Park, Young-Kweon,Kim, Gang-San,Kang, Byung-Ki,Ra, Ki-Ung 대한한방내과학회 2001 大韓韓方內科學會誌 Vol.22 No.1

Object : Hepatitis Treatment-tang No.1 has been used for the treatment of Liver disease and Jaundice. Long-term EtOH exposure leads to immunoregulatory and detoxification impairment. This study aimed to determine the relationship between TNF-${\alpha}$ production and expression, and EtOH-induced cytotoxicity on Hep G2 cells. Method : Cells were incubated with EtOH in the presence or absence of HT. The cells were tested after 24 hours and, again, after 48 hours. Cytoviability and TNF-${\alpha}$ release were analyzed by MTT assay and enzyme linked immunosorbent assay (ELISA), respectively. After 24 hours of EtOH exposure, the cytoviability decreased, and the release of TNF-${\alpha}$ was increased. Increased amounts of TNF-${\alpha}$ contribute to EtOH-induced cytotoxicity. The Anti-TNF-${\alpha}$ antibody almost abolished it. Interestingly, EtOH-induced cytotoxicity and TNF-${\alpha}$ production were inhibited by HT. Moreover, when HT was used in combination with the anti-TNF-${\alpha}$ antibody, there was a marked inhibition of EtOH-induced cytotoxicity. Results : These results suggest that HT may prevent the cytotoxicity through partial inhibition of the TNF-${\alpha}$ secretion.

Stearic acid, Oleic acid, Elaidic acid에 의한 간세포의 성장 및 지방산 조성의 변화

변부형 慶山大學校 1997 論文集 Vol.15 No.1

This study was carried out in order to investigate the effect of stearic acid (18:0,SA), oleic (18:1cis.0A) and elaidic acid (18:1 trans, EA) on the cell growth and fatty acid composition of Hep-G2 cells. The cells were incubated in serum-free medium 25, 50, 100 and 200uM of fatty acid combined with albumin for 2 days. The fatty acid concentration up to lOOuM showed the normal growth, but the cell growth decreased in the presence of 200uM fatty acid. The treatment of cells with lOOuM of a fatty acid for two days significantly (p<0.05) increased the cellular triglyceride (TG) content in all fatty acid groups compared to control, but TG content was not significantly different among all treatment group, but total cholesterol (TC) was the highest level in EA group. Cellular phospholipid(PL) contents were similar between the control and all faty acid groups.

Hepatoprotective Constituents of the Edible Brown Alga Ecklonia stolonifera on Tacrine-induced Cytotoxicity in Hep G2 Cells

Kim, Youn-Chul,An, Ren-Bo,Yoon, Na-Young,Nam, Taek-Jeong,Choi, Jae-Sue The Pharmaceutical Society of Korea 2005 Archives of Pharmacal Research Vol.28 No.12

In this study, ethanolic extracts from 18 seaweed variants were assessed for hepatoprotective activity against tacrine-induced cytotoxicity in Hep G2 cells. Only one of these, Ecklonia stolonifera Okamura (Laminariaceae), a member of the brown algae, exhibited promising hepatoprotective activity. Bioassay-guided fractionation of the active ethyl acetate (EtOAc) soluble fraction obtained from the ethanolic extract of E. stolonifera, resulted in the isolation of several phlorotannins [phloroglucinol (1), eckstolonol (2), eckol (3), phlorofucofuroeckol A (4), and dieckol (5)]. Compounds 2 and 4 were determined to protect Hep G2 cells against the cytotoxic effects of tacrine, with $EC_{50}$ values of 62.0 and 79.2 $\mu$g/mL, respectively. Silybin, a well characterized hepatoprotective agent, was used as a positive control, and exhibited an $EC_{50}$ value of 50.0 $\mu$g/mL. It has been suggested that the phlorotannins derived from marine brown algae might prove useful sources in the development of novel hepatoprotective agents.