• Title/Summary/Keyword: Hep G2

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Induction of apoptosis using the mixture of fucoidan and Crepidiastrum denticulatum extract in HepG2 liver cancer cells (후코이단/이고들빼기 혼합물에 의한 HepG2 간암세포의 apoptosis 유도)

  • Se-Eun Park;Dabin Choi;Kyo-nyeo Oh;Hanjoong Kim;Hyungbum Park;Ki-Man Kim
    • Food Science and Preservation
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    • v.31 no.2
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    • pp.276-286
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    • 2024
  • In the present study, we investigated whether a mixture of fucoidan and Crepidiastrum denticulatum extract (FCE) had the potential to improve the therapeutic efficacy of cancer treatment. The results demonstrated that FCE significantly reduced cell viability and induced the release of LDH (lactate dehydrogenase) and DNA fragmentation in HepG2 cells in a dose-dependent manner. In addition, FCE treatment also increased the protein expression level of p53, the release of cytochrome c, and the loss of mitochondrial membrane potential. Moreover, FCE dose-dependently increased protein expression levels of Bax, and cleaved caspase-3 and -9. However, FCE decreased the protein expression level of Bcl-2. These results suggest that FCE inhibits cell proliferation and induces apoptosis via the mitochondrial-mediated intrinsic pathway. The present study demonstrates that FCE can be used as an anti-cancer agent for liver cancer based on apoptosis mechanism.

In vitro Anticancer Effect of Salt on HepG2 Human Hepatocellular Carcinoma Cells (소금의 HepG2 인체 간암세포에서의 in vitro 항암 효과)

  • Kim, Hee-Young;Ju, Jaehyun;Lee, Kyung Hee;Park, Kun-Young
    • Journal of the Korean Society of Food Science and Nutrition
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    • v.45 no.1
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    • pp.137-142
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    • 2016
  • We investigated the anti-proliferative effects of solar salt and purified salt (PS) on HepG2 human hepatocellular cancer cells as well as their effects on mRNA and protein expression of apoptosis- and cell cycle-related genes, including Bcl-2, Bax, p53, and p21. Each salt sample suppressed cancer cell proliferation when treated at a concentration of 0.5% or 1%. Especially solar salt from T salt field (SS-T) and solar salt from Y salt field (SS-Y) significantly suppressed proliferation of cancer cells in comparison with PS. Treatment of HepG2 cells with salt samples at a concentration of 1% suppressed expression of Bcl-2 and promoted expression of Bax, p53, and p21 at the mRNA and protein levels in comparison with the control group. Inductively coupled plasma optical emission spectrometry (ICP-OES) showed that SS-T and SS-Y had higher concentrations of Ca, Mg, S, and K than PS, and SS-T contained higher concentrations of these minerals than SS-Y. It seems that Na and mineral contents in solar salt may contribute to regulation of the genes. Taken together, salt, especially mineral rich solar salt, inhibits cancer cell growth by regulating apoptosis and cell cycle-related genes.

Sanguinarine Induces Apoptosis in Human Hepatocellular Carcinoma HepG2 Cells through the Generation of ROS and Modulation of Akt/ERK Signaling Pathways (HepG2 인체 간암세포의 ROS 생성 및 ERK/Akt 신호전달 경로 조절을 통한 sanguinarine의 apoptosis 유도)

  • Hwang, Ju Yeong;Cho, Yung Hyun
    • Journal of Life Science
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    • v.25 no.9
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    • pp.984-992
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    • 2015
  • Sanguinarine is a benzophenanthridine alkaloid originally isolated from the roots of Sanguinaria canadensis. It has multiple biological activities (e.g., antioxidant and antiproliferative) and immune-enhancing potential. In this study, we explored the proapoptotic properties and modes of action of sanguinarine in human hepatocellular carcinoma HepG2 cells. Our results revealed that sanguinarine inhibited HepG2 cell growth and induced apoptosis in a dose-dependent manner. The induction of apoptosis by sanguinarine was associated with the up-regulation of Fas and Bax, the release of cytochrome c from the mitochondria to the cytosol, and the loss of the mitochondrial membrane potential. In addition, sanguinarine activated caspase-9 and -8, initiator caspases of the intrinsic and death extrinsic pathways, respectively, and caspase-3, accompanied by proteolytic degradation of poly (ADP-ribose) polymerase. Sanguinarine also triggered the generation of reactive oxygen species (ROS). The elimination of ROS by N-acetylcysteine reversed sanguinarine-induced apoptosis. Furthermore, sanguinarine induced the dephosphorylation of Akt and the phosphorylation of mitogen-activated protein kinases, including extracellular signal-regulated kinase (ERK), c-jun N-terminal kinase (JNK), and p38. The growth inhibition was enhanced by the combined treatment of sanguinarine with a phosphatidylinositol 3'-kinase (PI3K) inhibitor and an ERK inhibitor but not JNK and p38 inhibitors. Overall, our data indicate that the proapoptotic effects of sanguinarine in HepG2 cells depend on ROS production and the activation of both intrinsic and extrinsic signaling pathways, which is mediated by blocking PI3K/Akt and activating the ERK pathway. Thus, our data suggest that sanguinarine may be a natural compound with potential for use as an antitumor agent in liver cancer.

Effect of Zibachunggan-tang on lipopolysaccharide-induced expression of NF-kB downstream genes in HepG2 cell (자발 '청간탕'이 HepG2 cell의 염증반응에 대한 연구)

  • Hong Sang Hoon;Choi Byung Tae;Lee Yong Tae
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.17 no.5
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    • pp.1251-1256
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    • 2003
  • To determine the effect of Zibachunggan-tang(ZCT) on the process of lipopolysaccharide (LPS)-induced nuclear factor-kBp65 (NF-kBp65) activation, and LPS-induced expression of pro-inflammatory proteins including tumor necrosis factor-α (TNF-α), nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), in HepG2 cell. Immunoblot analysis showed that the level of nucleic NF-kBp65 was rapidly up-regulated and cytosolic inhibitory I-kBα was down-regulated by LPS challenge. While ZCT inhibited an increase of NF-kBp65 and degradation of I-kBα in HepG2 cell. Beside LPS-induced expression of a group of genes, such as TNF-α, inducible iNOS and COX-2, are repressed by ZCT. It may be concluded that ZCT attenuates the progress of LPS-induced inflammation by reduction of NF-kBp65 activation. The ZCT would be useful as a therapeutic agent for endotoxin-induced liver disease.

Anticarcinogenic and Antioxidant Effects of Rhodiola sachalinensis (홍경천의 항산화 · 항발암 효과 연구)

  • Bae, Song-Ja
    • Journal of the Korean Society of Food Science and Nutrition
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    • v.34 no.9
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    • pp.1302-1307
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    • 2005
  • In this study, we investigated the anticarcinogenic and antioxidative activities of Rhodiola sachalinensis (RS). Hexane (RSMH), ethylether (RSMEE), ethylacetate (RSMEA), butanol (RSMB), aqueous (RSMA) fractions and methanol extract (RSM) were screened for their growth inhibition effects using 3- (4,5-dimethyl-thiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay on HepG2, HeLa, MCF-7 and HT-29 cells. The anticarcinogenic effects of RSMEE was most significant when tested on MCF-7 and HepG2 cell lines at the concentration of $500{\mu}g/mL$ which resulted about $84\%\;and\;90\%$ on MCF-7 and HepG2 cells, respectively. The quinone reductase (QR)-inducing activity of RSMH on HepG2 cells was 3.5 times higher compared with the control at the concentration of $200{\mu}g/mL$. Antioxidative activities of RSM, RSMEE, RSMEA and RSMB showed about $80\%$ of electron donating activity (EDA) which were very similar to that of vitamin C as a control. We observed morphological changes of shrinking and the blebbing of HepG2 cancer cell membranes depending on the concentration of RSMEE.

Kaurenoic acid, a natural substance from traditional herbal medicine, alleviates palmitate induced hepatic lipid accumulation via Nrf2 activation

  • Han, Changwoo
    • The Journal of Korean Medicine
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    • v.41 no.4
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    • pp.64-71
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    • 2020
  • Objectives: This study was done to look into whether Nrf2 take some role in the anti-lipogenic effect of kaurenoic acid in a nonalcoholic fatty liver disease (NAFLD) cellular model. Materials and Methods: We measured the effect of kaurenoic acid on intracellular steatosis and Nrf2 activation. Next, the effect of kaurenoic acid on SREBP-1c and some lipogenic genes in palmitate treated HepG2 cells with or without Nrf2 silencing. Results: The increased SREBP-1c expression was significantly decreased by concomitant kaurenoic acid treatment in non-targeting negative control siRNA transfected HepG2 cells. However, kaurenoic acid did not significantly inhibited increased SREBP-1c level in Nrf2 specific siRNA transfected HepG2 cells Conclusions: Kaurenoic acid has a potential to activate Nrf2, which may suppress SREBP-1c mediated intracellular steatosis in HepG2 cells.

HepG2 세포의 산화적 손상에 대한 산삼 추출물의 보호효과 - DNA chip을 이용하여 -

  • Kim, Hyung-Seok;Park, Hee-Soo;Kwon, Ki-Rok
    • Journal of Pharmacopuncture
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    • v.10 no.1 s.22
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    • pp.121-135
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    • 2007
  • Objectives : This study was carried out to examine protective effect of wild ginseng extract on HepG2 human hepatoma cell line against tert-Butyl hydroperoxide (t-BHP)-induced oxidative damage. Methods : To evaluate protective effect of wild ginseng extract against t-BHP induced cytotoxicity, LDH level and activity of glutathione peroxidase and reductase were measured. Gene expression was also measured using DNA microarray. Results : Wild ginseng extract showed a significant protective effect against t-BHP-induced cytotoxicity in HepG2 cell line. It is not, however, related with the activities of glutathione peroxidase and glutathione reductase. Analysis of gene expression using DNA chip, demonstrated that 28 genes were up-regulated in t-BHP only group. Five genes - selenoprotein P, glutathione peroxidase 3, sirtuin 2, peroxiredoxin 2, serfiredoxin 1 homolog - may be related with the protective effect of wild ginseng extract. Conclusions : Based on the results, a protective effect of wild ginseng extract against t-BHP-induced oxidative damage in HepG2 cell line is not associated with the activities of glutathione peroxidase and glutathione reductase, but with the expression of selenoprotein P, glutathione peroxidase 3, sirtuin 2, peroxiredoxin 2, and serfiredoxin 1 homolog.

Anti-proliferating Effects of Porphyra tenera Fractions on Several Cancer Cell Lines in uitro (김 분획물의 in vitro에서의 항발암효과)

  • Shin, Mi-Ok;Bae, Song-Ja
    • Journal of the Korean Society of Food Science and Nutrition
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    • v.34 no.10
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    • pp.1514-1519
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    • 2005
  • This study was performed to investigate the effects of Porphyra tenera (PT) on cytotoxicity and quinone reductase (QR) activity in the cancer cells. PT was extracted with methanol and further fractionated into five different types: hexane (PTMH), ethyl-ether (PTMEE), ethylacetate (PTMEA) butanol (PTMB) and aquous (PTMA) partition layers. We determined the cytotoxic effect of these layers on C6, HepG2, MCF-7, and HT-29 cell lines by MTT assay. Among the various fractions, hexane (PTMH) of PT showed the strongest cytotoxic effect on C6, HepG2 and MCF-7 cell lines. PTMH displayed very low level of cytotoxicity at the lower concentration levels and at 300 $\mu$g/mL. PTMH resulted in 87.5$\%$ growth inhibition on C6 cell 70 $\%$ on the HepG2 cell and 89$\%$ on the MCF-7 cell, which were significantly high compared to other fractions. A 400 $\mu$g/mL PTMH concentration level, 99$\%$, 94.5$\%$ and 99$\%$ of cell growth inhibition were resulted on the same cell lines. On HT-29 cell line, both hexane (PTMH) and aqueous (PTMA) fraction of PT showed cytotoxic effects, but the Percentage was not as high as previous results tested on other cell lines such as C6 HepG2 and MCF-7 cell lines. Also, we observed quinone reductase (QR) inducing-effects in all fractions of PT on HepG2 cells. The QR inducing effects of the PTMH on HepG2 cells at 150 $\mu$g/mL concentration was 6.6 times higher than the control. Although further studies are needed, the present work suggests that PT was a potential to be used as a chemopreventive.

Induction of Apoptosis by Bile Acids in HepG2 Human Hepatocellular Carcinoma Cells

  • Baek, Jin-Hyen;Kim, Jung-Ae;Kang, Chang-Mo;Lee, Yong-Soo;Kim, Kyu-Won
    • The Korean Journal of Physiology and Pharmacology
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    • v.1 no.1
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    • pp.107-115
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    • 1997
  • We studied the effects of bile acids on the induction ofapoptosis in HepG2 human hepatocellular carcinoma cells. Treatment with either ursodeoxycholic acid (UDCA) or lithocholic acid (LCA) resulted in a dose- and time-dependent decrease in cell viability assessed by MTT assay. Both UDCA and LCA also induced genomic DNA fragmentation, a hallmark of apoptosis, indicating that the mechanism by which these bile acids induce cell death was through apoptosis. Cycloheximide, a protein synthesis inhibitor, blocked the apoptosis induced by these bile acids, implying that new protein synthesis may be required for the apoptosis. Intracellular $Ca^{2+}$ release blockers (dantrolene and 3,4,5-trimethoxybenzoic acid-8-(diethylamino)octyl ester) inhibited decreased cell viability and DNA fragmentation induced by these bile acids. Treatment of HepG2 cells with calcium ionophore A23l87 induced DNA fragmentation. These results suggest that UDCA and LCA induce apoptosis in the HepG2 cells and that the activation of intracellular $Ca^{2+}$ signals may play an important role in the apoptosis induced by these bile acids.

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(β-lapachone Regulates Tight Junction Proteins, Claudin-3 and -4, in Human Hepatocarcinoma Cells. (인체 간암세포에서 β-lapachone 처리에 의한 Tight Junction 관련 유전자의 변화)

  • Kim, Sung-Ok;Kwon, Jae-Im;Kim, Gi-Young;Kim, Nam-Deuk;Choi, Yung-Hyun
    • Journal of Life Science
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    • v.17 no.9 s.89
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    • pp.1298-1302
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    • 2007
  • A hallmark of cancers is 'leaky' tight junctions (Tjs). TJs mediated paracellular permeability is elevated and TJs maintained cell polarity is frequently lost. Concomitantly, TJs-associated proteins including members of the claudin family of proteins are dysregulated. Recent findings indicate that these TJs changes can contribute to cancer progression. In this study, we examined the effects of ${\beta}-lapachone$, a quinone compound obtained from the bark of the lapacho tree (Tabebuia avellanedae), on the Tjs-associated regulators in human hepatocarcinoma cell lines, HepG2 and Hep3B. ${\beta}-lapachone$ treatment downregulated the levels of insulin-like growth factor 1 receptor (IGF-lR) proteins in both HepG2 and Hep3B cells. But the levels of claudin-3 and -4 proteins were increased in ${\beta}-lapachone$-treated HepG2 and Hep3B cells. And also the zonnula occludens-l (la-I) and p-catenin protein levels by ${\beta}-lapachone$ were increased in a time-dependent manner. However, claudin-3 and -4 mRNA levels were uninhibited by ${\beta}-lapachone$ in HepG2 and Hep3B. The present results suggest that the upregulation of claudin-3 and -4 protein levels by ${\beta}-lapachone$ occurs by a post-transcriptional mechanism and points to a novel mechanism by ${\beta}-lapachone$.