• Journal of the Korean Society of Food Science and Nutrition
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• v.36 no.1
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• pp.8-13
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• 2007

This study was conducted to investigate the effect of mycelia of Lentinus edoes mushroom-cultured Astragalus membranaceus Bunge (LAM) on proliferation of cancer cell lines (Hep3B, MCF-7 and HeLa), sarcoma 180 (S-180), and anti-allergy. In an anti-cancer test using Hep3B (hepatic cancer cell), MCF-7 (breast cancer cell) and HeLa (uterine cancer cell), LAM extract showed higher antiproliferating effect than that of Astragalus membranaceus Bunge (AM) extract. In an anti-cancer testing using Hep3B cells and MCF-7 cells, LAM extract showed growth-inhibitory effect of 65.23% at 3 mg/mL and 69.23% at 5 mg/mL, respectively. In an anti-cancer testing using HeLa cells, LAM extract showed growth-inhibitory effect of 42.01% at 5 mg/mL. In addition, LAM showed the tumor suppressive effect in mice injected with S-180 cells. The growth-inhibitory rates against tumor cells were 47% for LAM and 37% for AM. LAM inhibited histamine release from rat peritoneal mast cells activated by compound 48/80. These results suggest that Lentinus edodes mushroom-cultured herb has an antiproliferating effect against cancer cell lines (Hep3B, MCF-7 and HeLa), S-180 tumor and will be beneficial in the treatment of allergic reaction.

• Journal of the Korean Society of Food Science and Nutrition
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• v.36 no.4
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• pp.424-430
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• 2007

This study was conducted to investigate the effect of mycelia of Lentinus edoes mushroom-cultured Lonicera japonica Thunberg (LLJ) on proliferation of the cancer cell lines (Hep3B, MCF-7 and HeLa), sarcoma 180 (S-180) and antiallergy. In an anti-cancer test using Hep3B (hepatic cancer cell), MCF-7 (breast cancer cell) and HeLa (uterine cancer cell), LLJ extract showed higher antiproliferating effect than that of LJ (Lonicera japonica Thunberg) extract. In an anti-cancer testing using Hep3B cells, LLJ extract showed growth-inhibitory effect of $85.60{\pm}4.66%$ at 3mg/rnL. In an anti-cancer testing using MCF-7 cells, LLJ and LJ extracts showed high antiproliferating effect. LLJ showed the tumor suppressive effect in mice injected with S-180 cells. The growth-inhibitory rates against tumor cells were 61% for LLJ, 37% for LJ. LLJ inhibited histamine release from rat peritoneal mast cells activated by compound 48/80. These results suggest that Lentinus edodes mushroom-cultured herb has an antiproliferating effect against cancer cell lines (Hep3B, MCF-7 and HeLa) and S-180 tumor, and will be beneficial in the treatment of allergic reaction.

• Journal of Life Science
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• v.26 no.7
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• pp.764-771
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• 2016

Extracts from Artemisia annua Linné (AAE) have been known to possess various functions, including anti-bacterial, anti-virus, and anti-oxidant effects. However, the mechanism of those effects of AAE is not well-known. The aim of this study was to analyze the inhibitory effects of AAE on cell proliferation of the human hepatoma cell line (Hep3B) and to examine its effects on apoptosis. Activation by phosphorylation of Akt is cell proliferation through the phosphorylation of TSC2, mTOR, and GSK-3β. We suggested that AAE may exert cancer cell apoptosis through Akt/mTOR/GSK-3β signal pathways and mitochondria-mediated apoptotic proteins. For this, we examined the effects of extracts of AAE on cell proliferation according to treatment concentration. Treatment with AAE not only reduced cell viability, but also resulted in the induced release of lactate dehydrogenase (LDH). These results were determined with a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and a lactate dehydrogenase (LDH) assay. Furthermore, we determined the effects of apoptosis through Hoechst 33342 staining, annexinⅤ-propidium iodide (PI) staining, 5,5′, 6,6′-tetrachloro-1,1′,3,3′-tetraethyl-imidacarbocyanine iodide (JC-1) staining, and Western blotting. Our study showed that the treatment of liver cancer cells with AAE resulted in the inhibition of Akt, TSC2, GSK-3β-phosphorylated, Bcl-2, and pro-caspase 3 and the activation of Bim, Bax, Bak, and cleaved PARP expressions. These results indicate that AAE induced apoptosis by means of a mitochondrial event through the regulate of Akt/mTOR/GSK-3β signaling pathways.

• The Journal of Internal Korean Medicine
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• v.26 no.1
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• pp.74-92
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• 2005

Objectives/Methods : To analyze the effect of Injinchunggantang(IJCGT) to Interferon-${\alpha}/{\beta}$ signal transmission system in HepG2 cells, HepG2 Cell were treated with IJCGT. Also, revelation of MxA, 2'5'-OAS mRNA leaded by Interferon-${\alpha}/{\beta}$ and revelation and activation of Jak1, TYK1, and STAT 1, all main signal transmission factors, were analyzed. Results : The analysis resulted in the following 1. With interferon ${\alpha}/{\beta}$ there was no affect cell propagation of Hep G2 cells. With IJCGT alone, cell propagation of HepG2 was promoted, and cell propagation control function was recovered. 2. With interferon ${\alpha}/{\beta}$ cell death was unaffected. With IJCGT apoptosis of HepG2 cell was restrained, and the cell's reaction to interferon was unaffected. 3. With interferon ${\alpha}/{\beta}$ treatment mRNA revelation of MxA and 2'5'-OAS was induced. When HepG2 cells were injected with IJCGT without interferon ${\alpha}/{\beta}$ treatment, mRNA revelation of MxA and 2'5'-OAS increased in proportion to the treatment density. With pre-treatment of IJCGT, leaded with interferon ${\alpha}/{\beta}$, promoted revelation of MxA, 2'5' -OAS mRNA. 4. Though mRNA revelation of lakl, TYK1 and STAT1 was unaffected with IJCGT, activation of STAT1 was promoted with an increase of phosphorylation of STAT1 protein. With pre-treatment of IJCGT, Jak1, TYK2, STAT1 phosphorylation, leaded with interferon, strengthened. 5. TNF-a, IL-1b and LPS present, revelation of MxA and 2'5'-OAS mRNA leaded by interferon was restrained when HepG2 cells were treated with IJCGT, and the interferon signal transmission system restraint action leaded by inflammatory cytokines was moderated. Conclusion : These results support a role for IJGCT in promotion of anti-virus action through maintainance of the liver's sensibility toward interferon. A clinical study of an interferon treated patient treated also with IJGCT is needed to determine its efficacy.

• Journal of Nutrition and Health
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• v.27 no.9
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• pp.910-923
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• 1994

The effects of individual fatty acids, differing in their degree of unsaturation(18:0, 18:1, 18:2 and 18:3) on the biosynthesis and secretion and lipids were investigated in Hep-G2 cells. Synthesis of apolipoprotein was measured by the incorporation of 3H-leucine into apolipoprotein(d<1.21g/ml) and synthesis of lipids was measured by the incorporation of 3H-glycerol and 14C-acetate into various lipid classes. Inclusion of 1.0mM of each fatty acids into the culture medium significantly increased the synthesis of total apolipoprotein and Apo B(p<0.05). However, addition of fatty acid did not affect the synthesis of cellular and medium protein. Among different fatty acids tested, oleic acid had the greatest effect on Apo B synthesis. While stearic, linoleic and linolenic acid, all had similar effects. The secretion of triglyceride into the medium markedly increased in all fatty acid groups being 5-6 times over the albumin control. The triglyceride secretion was the highest int he oleic acid group. The secretion of phospholipid and cholesterol also increased with triglyceride output. A positive relationship existed between the output of lipoprotein-triglyceride and Apo B. Since the synthesis of Apo B was significantly increased when various fatty acids were included into the culture medium, part of the apparently stimulated synthesis of the apolipoprotein may be in response to the increased formation and secretion of lipoprotein lipids.

• Korean Journal of Food Science and Technology
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• v.46 no.3
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• pp.384-389
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• 2014

The objective of the present study was to investigate the chemical composition of anthocyanin-enriched extract of radiation-induced blackberry (Rubus fruticosus L.) mutant (${\gamma}$-B201) as well as the protective effect of ${\gamma}$-B201 against oxidative stress in vitro. The cytotoxicity, reactive oxygen species (ROS) scavenging capacity, and DNA damage were assessed by WST-1 assay, flow cytometry, and comet assay, respectively. Lactate dehydrogenase, superoxide dismutase, and catalase activities were determined by using a commercial kit. The in vitro results showed that ${\gamma}$-B201 increased the cell viability, reduction of lactate dehydrogenase release, and intracellular ROS scavenging capacity in hydrogen peroxide ($H_2O_2$)-treated HepG2 cells. Furthermore, treatment with ${\gamma}$-B201 attenuated DNA damage in $H_2O_2$-treated HepG2 cells and treatment with ${\gamma}$-B201 restored the activity of superoxide dismutase and catalase in $H_2O_2$-treated HepG2 cells. In conclusion, the present study suggests that ${\gamma}$-B201 blackberry extract can exert a significant cytoprotective effect against $H_2O_2$-induced cell damage.

• BMB Reports
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• v.46 no.10
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• pp.513-518
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• 2013

We investigated the protective effects of Gymnaster koraiensis against oxidative stress-induced hepatic cell damage. We used two different cytotoxicity models, i.e., the administration of tert-butyl hydroperoxide (t-BHP) and acetaminophen, in HepG2 cells to evaluate the protective effects of G. koraiensis. The ethyl acetate (EA) fraction of G. koraiensis and its major compound, 3,5-di-O-caffeoylquinic acid (DCQA), exerted protective effects in the t-BHP-induced liver cytotoxicity model. The EA fraction and DCQA ameliorated t-BHP-induced reductions in GSH levels and exhibited free radical scavenging activity. The EA fraction and DCQA also significantly reduced t-BHP-induced DNA damage in HepG2 cells. Furthermore, the hexane fraction of G. koraiensis and its major compound, gymnasterkoreayne B (GKB), exerted strong hepatoprotection in the acetaminophen-induced cytotoxicity model. CYP 3A4 enzyme activity was strongly inhibited by the extract, hexane fraction, and GKB. The hexane fraction and GKB ameliorated acetaminophen-induced reductions in GSH levels and protected against cell death.

• Journal of the Korean Society of Food Science and Nutrition
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• v.29 no.2
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• pp.322-328
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• 2000

This study was performed to determine the antimutagenic and cytotoxic effect of the Phellinus linteus methanol extract on Salmonella typhimurium TA98, TA100 and human cancer cell lines. In the Ames test, methanol extract of P. linteus alone did not exhibit any mutagenicity but showed substantial inhibitory effects against mutation induced by N-methyl-N'-nitro-N-nitrosoguanidine(MNNG), 4-nitroquinoline-nitroquinoline-1-oxide(4NQO), 3-amino-1,4-dimethyl-5H-pyrdo[4,3-blindol(Trp-P-1) and benzo(α)pyrene(B(α)P). The methanol extracts of P. linteus(200㎍/plate) showed approximately 78.3%, 78.7% and 88.1% inhibitory effect on the mutagenesis induced by 4NQO, Trp-P-1 and B(α)P. The anticancer effects of P. linteus extract against human breast adenocarcinoma(MCF7), human lung carcinoma (A549), human fibrosarcoma (HT1080), human hepatocelular carcinoma (Hep3B) and human epitheloid carcinoma (HeLa) were investigated. The treatment of 1mg/mL P. linteus extracts had the highest cytotoxicity against MCF7 (92.0%), followed by Hep3B (84.9%), A549 (84.2%) and HT1080 (82.9%). In contrast 1mg/mL treatment of P. linteus extracts had only 10∼40% cytotoxicity on normal human liver cell (WRL68).

• International Journal of Oral Biology
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• v.45 no.4
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• pp.169-178
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• 2020

L-ascorbic acid (L-AA; vitamin C) induces apoptosis in cancer cells. This study aimed to elucidate the molecular mechanisms of L-AA-induced apoptosis in human laryngeal epidermoid carcinoma Hep-2 cells. L-AA suppressed the viability of Hep-2 cells and induced apoptosis, as shown by the cleavage and condensation of nuclear chromatin and increased number of Annexin V-positive cells. L-AA decreased Bcl-2 protein expression but upregulated Bax protein levels. In addition, cytochrome c release from the mitochondria into the cytosol and activation of caspase-9, -8, and -3 were enhanced by L-AA treatment. Furthermore, apoptosis-inducing factor (AIF) and endonuclease G (EndoG) were translocated into the nucleus during apoptosis of L-AA-treated Hep-2 cells. L-AA effectively inhibited the constitutive nuclear factor-κB (NF-κB) activation and attenuated the nuclear expression of the p65 subunit of NF-κB. Interestingly, L-AA treatment of Hep-2 cells markedly activated Akt and mitogen-activated protein kinase (MAPK; extracellular signal-regulated kinase 1/2, p38, and c-Jun N-terminal kinase [JNK]) and and LY294002 (Akt inhibitor), SB203580 (p38 inhibitor) or SP600125 (a JNK inhibitor) decreased the levels of Annexin V-positive cells. These results suggested that L-AA induces the apoptosis of Hep-2 cells via the nuclear translocation of AIF and EndoG by modulating the Bcl-2 family and MAPK/Akt signaling pathways.

• Fisheries and Aquatic Sciences
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• v.26 no.2
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• pp.133-144
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• 2023

Auranofin is a US Food and Drug Administration (FDA)-approved anti-arthritis medication that functions as a thioredoxin reductase inhibitor. Spermidine, a polyamine present in marine algae, can exert various physiological functions. Herein, we examined the synergistic anticancer activity of auranofin and spermidine in hepatocellular carcinoma (HCC). Combined treatment with auranofin and spermidine suppressed cell viability more efficiently than either treatment alone in HCC Hep3B cells. The isobologram plotted by calculating the half maximal inhibitory concentration (IC₅₀) values of each drug indicated that the two drugs exhibited a synergistic effect. Based on the analysis of annexin V and cell cycle distribution, auranofin and spermidine markedly induced apoptosis in Hep3B cells. Moreover, auranofin and spermidine increased mitochondria-mediated apoptosis by promoting mitochondrial membrane potential (Δψm) loss. Auranofin and spermidine significantly increased reactive oxygen species (ROS) production in Hep3B cells, and the blocking ROS suppressed apoptosis induced by spermidine and auranofin. In addition, auranofin and spermidine reduced the expression of phosphorylated phosphatidylinositol-3 kinase (PI3K) and protein kinase B (Akt), and PI3K inhibitor accelerated auranofin- and spermidine-induced apoptosis. Using ROS scavenger and PI3K inhibitor, we revealed that ROS acts upstream of auranofin- and spermidine-induced apoptosis. Collectively, our study suggests that combination treatment with auranofin and spermidine could afford synergistic anticancer activity via ROS overproduction and reduced PI3K/Akt signaling pathway.