• The Korea Journal of Herbology
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• v.30 no.1
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• pp.33-42
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• 2015

Objectives : The aim of this study was to evaluate the antitumor effects of Cheongpyesagan-tang(CST) and YKK012 on colon cancer. Methods : MTT assay was used to evaluate the cytotoxicity of Single herbs and combinations of CST and YKK012 on murine colon cancer cells, Colon 38. To explain effects of apoptosis in colon cancer, we performed the western blot. Effects of CST and YKK012 on antitumor activity of CPT-11 using the murine colon38 allograft tumor in BDF1 mice. Results : Single herbs and combinations of CST and YKK012 was tested in vitro, Rhei Radix (RH) and Scutellariae Radix (SC) and YKK012 showed dose-response cytotoxicity on Colon 38. This might be due to the apoptosis, as we see Bax and Caspase-3, which are apoptotic factors, was expressed in RH and SC treated cells. YKK012 also showed increased expression of Caspase-3. In mouse colorectal cancer xenograft model of colon38 cells, herbal combinations showed tendencies of tumor regression, but was not significant. Furthermore, because toxicity was observed in CST group, we reduced the dose of CST for the next experiment. The anti-tumor effects of herbal combinations were insufficient to be used as single anti-tumor agent. With simultaneous usage of CPT-11, contrary to that CST showed no synergistic effects, YKK012 which was composed by the combination of four $ER{\beta}$ selective herbs, significantly reduced the size of tumor and Bax expression was increased. Conclusions : We suggest YKK012 can be a effective cancer adjuvant therapy with CPT-11 on colon cancer.

• BMB Reports
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• v.48 no.7
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• pp.395-400
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• 2015

Parkinson's disease (PD) is a neurodegenerative disability caused by a decrease of dopaminergic neurons in the substantia nigra (SN). Although the etiology of PD is not clear, oxidative stress is believed to lead to PD. Catalase is antioxidant enzyme which plays an active role in cells as a reactive oxygen species (ROS) scavenger. Thus, we investigated whether PEP-1-Catalase protects against 1-methyl-4-phenylpyridinium (MPP⁺) induced SH-SY5Y neuronal cell death and in a 1-methyl-4-phenyl-1,2,3,6-trtrahydropyridine (MPTP) induced PD animal model. PEP-1-Catalase transduced into SH-SY5Y cells significantly protecting them against MPP⁺-induced death by decreasing ROS and regulating cellular survival signals including Akt, Bax, Bcl-2, and p38. Immunohistochemical analysis showed that transduced PEP-1-Catalase markedly protected against neuronal cell death in the SN in the PD animal model. Our results indicate that PEP-1-Catalase may have potential as a therapeutic agent for PD and other oxidative stress related diseases. [BMB Reports 2015; 48(7): 395-400]

• KSBB Journal
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• v.24 no.5
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• pp.446-452
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• 2009

Oleyl alcohol, butyl butyrate, and two different ionic liquids were evaluated for the extraction of butanol from culture broth without toxic effect to cells. The tested solvents showed more than 50% extraction efficiency, and oleyl alcohol was chosen as the best extractant for butanol among the used extractants with a partition coefficient of 2.89. When oleyl alcohol was used as an extractant, more than 80% of butanol was extracted in the wide range of butanol concentrations (1-20 g/L) and pH values (pH 4-5.5). In extractive fermentation using oleyl alcohol only, there was 11% more butanol production and glucose consumption when compared to that without extractive fermentation, implicating a reduced inhibitory effect of butanol due to butanol removal to the oleyl alcohol phase. In addition, oleyl alcohol did not inhibit cell growth, while a mixture of oleyl alcohol and butyl butyrate with the volume ratio of 9:1~7:3 inhibited either butanol production or cell growth significantly due to the toxicity of butyl butyrate to cells. In conclusion, oleyl alcohol can be used as an efficient and non-toxic solvent for extractive fermentation for butanol production.

• Journal of Life Science
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• v.22 no.8
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• pp.1052-1056
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• 2012

Undaria pinnatifada has been used as a natural diet food with few calories and as a source of iodine. Even though U. pinnatifida has been regarded as a diet food, the mechanisms of its inhibitory effects on adipocyte differentiation and the accumulation of fat in adipocytes are poorly understood. In this study, the effect and mechanism of U. pinnatifida ethanol extract on 3T3-L1 differentiation into adipocytes were investigated. The effects of U. pinnatifida ethanol extract on cell viability and the anti-adipogenic effect were investigated via MTT assay, Oil red O staining, RT-PCR, and western blot. The U. pinnatifida ethanol extract did not show toxicity up to a concentration of 50 ${\mu}g/ml$. The addition of U. pinnatifida ethanol extract decreased triglyceride contents by 40% when 50 ${\mu}g/ml$ of U. pinnatifida ethanol extract was added during 3T3-L1 differentiation and adipocyte triglyceride formation. The transcription and expression of peroxisome proliferator-activated receptor ${\gamma}$ ($PPAR{\gamma}$), leptin, and hormone-sensitive lipase (HSL) as adipocyte-specific proteins were determined by RT-PCR and western blot. The overexpression of $PPAR{\gamma}$ could accelerate adipocyte differentiation. Also, leptin was secreted for triglyceride accumulation in the adipocytes and the increase of adipocyte cell size. Thus, $PPAR{\gamma}$ and leptin were used as indicators of obesity. $PPAR{\gamma}$ and leptin were repressed by the increased addition of U. pinnatifida ethanol extract. This indicates that U. pinnatifida was effective as an anti-obesity agent by repressing the differentiation of 3T3-L1 into adipocytes and inhibiting triglyceride formation in adipocytes.

• Korean Journal of Food Science and Technology
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• v.31 no.3
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• pp.831-837
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• 1999

Ochratoxin A (OA), a naturally occurring mycotoxin, has been known to cause renal and hepatic lesion in human and animals. This study was carried out to investigate the modulation effects of antioxidant vitamins on OA-induced lipid peroxidation associated with oxidative damage. Vitamin C (10 mg/kg/day) and vitamin E (63.8 mg/kg/day) were administered by intraperitoneal (i.p.) injection to male ICR mice, and 1 hr later, OA which was dissolved in 0.1 M $NaHCO_3$, treated 4 mg/kg/day by i.p. injection. During 4 days repeated, and then measured superoxide dismutase (SOD) activity, catalase activity and malondialdehyde (MDA) formation in microsomes of liver and kidney. Additionally, the relationship between cell damage and modulation effects of antioxidant vitamins was evaluated by comet assay. Results were as followed; i) SOD, catalase activity and MDA level were significantly increased by OA treated, ii) SOD, catalase activity and MDA formation were significantly decreased by antioxidant vitamins combine treated, iii) blood cell damage associated with lipid peroxidation, induced by OA, also modulated by antioxidant vitamins. These results indicated that antioxidant vitamins might be used for prevention of renal and hepatic damage due to ochratoxicosis.

• Journal of fish pathology
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• v.21 no.1
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• pp.45-56
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• 2008

This study was conducted to find out biological responses of bivalves exposed to organotin compound.The results of the study confirmed that tribultyltin chloride (TBTCl) induce reduction of survival rate andburrowing activity, and histopathological feature in the foot structure of the equilateral venus, Gomphinaveneriformis. The experimental period was 36 weeks. The experimental groups consisted of a control and 3TBTCl exposure groups (0.4, 0.6, 0.8 ym TBTCl L'). The survival rate and burrowing activity were record-ed daily. For histological analysis, foot tissues were fixed in Bouin' s fluid and then stained H-E stain, AB-PAS (PH 2.5) reaction and Masson's trichrome stain after having serially sectioned the tissue by paraffinmethod at thickness of 4-6 ym. The survival rate was not significantly different between the control andexposure groups for 20 weeks, but in 0.8 Um TBTCl L', it was on the decreased ever since the exposure. Theburrowing activity was not significantly different in the exposure group compared to the control up to 12weeks, but in 0.6 and 0.8 ym TBTCl L', it measured the lowest level after 20 weeks. The foot is composedof the epidermal layer, connective tissue, and muscular layer. The epidermal layer is composed of simplecolumnar, cuboidal epithelia and mucous cells. The cilia were well developed on the apical surface ofepithelium, Circular, longitudinal and transverse muscle bundle were well developed in the muscular layer.The majority mucous cells showed blue color (542c) when it subjected to AB-PAS (PH 2.5) reaction. Nohistopathological alterations in the foot were observed up to 12 weeks. After 20 weeks of exposure to 0.8 (anTBTCl L'', the foot samples of exposed G. veneriformis showed disappearance of cilia and striated borderpartially and extension of hemolymph sinus. The mucous cell increased in the marginal of foot. At 28-weekof exposure to 0.4 ym TBTCl L', it observed weekly acid (564c), neutral (264c) and mixed mucous cell. At36-week of exposure to 0.6 ym TBTCl L', it showed fragmentation of the muscle and collagen fiber bundle,and also diappearance of cilia on epithelia and edema of epithelium in 0.8 ym TBTCl L''.

• Korean Journal of Pharmacognosy
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• v.47 no.3
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• pp.264-272
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• 2016

This study was carried out to evaluate the preventive effect of the Corni Fructus (SSU) 50 % EtOH extract (SSU-E50) against bisphenol A (BPA) toxicity in Leydig cells and improving testosterone deficiency syndrome in orchidectomized Sprague-Dawly (SD) rats. Antioxidant properties were measured by radical scavenging activity of SSU-E50 in ABTS assay and DPPH assay. Also, real-time polymerase chain reaction(real-time PCR) was performed to quantify the mRNA expression levels of antioxidant enzyme. SD rats were divided into eight group: normal, sham operation (Sham), orchidectomized (ORX), ORX treated with testosterone 1 mg/kg (Tes. 1), ORX treated with SSU water extract 100 mg/kg (SSU-A 100) and 300 mg/kg (SSU-A 300), ORX treated with SSU 50 % EtOH extract 100 mg/kg (SSU-E 100) and 300 mg/kg (SSU-E 300). On a comparative basis, the SSU showed better activity quenching ABTS with an IC50 value of 0.29 mg/ml and DPPH with an IC50 value of 0.33 mg/ml. Cell viability was evaluated by MTS assay as described not cytotoxic at the highest concentration of $500{\mu}g/ml$. Cytotoxicity of BPA showed in $200{\mu}M$, but definitely survived by treatment with SSU in Leydig cells. In addition, SSU increased the mRNA expression levels of antioxidant enzyme in BPA induced Leydig cells. Superoxide dismutase (SOD) level was slightly increased and malondialdehyde (MDA) level was decreased with SSU-A 100 in in-vivo. These results suggest that Corni Fructus extracts have the greatest property as a natural anti-oxidative and improves testosterone deficiency syndrome source.

• Biomolecules & Therapeutics
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• v.26 no.5
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• pp.439-445
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• 2018

T-type calcium channels are low voltage-activated calcium channels that evoke small and transient calcium currents. Recently, T-type calcium channels have been implicated in neurodevelopmental disorders such as autism spectrum disorder and neural tube defects. However, their function during embryonic development is largely unknown. Here, we investigated the function and expression of T-type calcium channels in embryonic neural progenitor cells (NPCs). First, we compared the expression of T-type calcium channel subtypes (CaV3.1, 3.2, and 3.3) in NPCs and differentiated neural cells (neurons and astrocytes). We detected all subtypes in neurons but not in astrocytes. In NPCs, CaV3.1 was the dominant subtype, whereas CaV3.2 was weakly expressed, and CaV3.3 was not detected. Next, we determined CaV3.1 expression levels in the cortex during early brain development. Expression levels of CaV3.1 in the embryonic period were transiently decreased during the perinatal period and increased at postnatal day 11. We then pharmacologically blocked T-type calcium channels to determine the effects in neuronal cells. The blockade of T-type calcium channels reduced cell viability, and induced apoptotic cell death in NPCs but not in differentiated astrocytes. Furthermore, blocking T-type calcium channels rapidly reduced AKT-phosphorylation (Ser473) and $GSK3{\beta}$-phosphorylation (Ser9). Our results suggest that T-type calcium channels play essential roles in maintaining NPC viability, and T-type calcium channel blockers are toxic to embryonic neural cells, and may potentially be responsible for neurodevelopmental disorders.

• Korean Journal of Environmental Biology
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• v.24 no.1 s.61
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• pp.46-52
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• 2006

The mercury is among the most highly bioconcentrated toxic trace metals. Many national and international agencies and organisations have targeted mercury for the possible emission control. The mercury toxicity depends on its chemical form, among which alkylmercury compounds are the most toxic. A human cervix uterus cancer cell line HeLa cells was employed to investigate the effect of the toxic heavy metal mercury (Hg) and ionizing radiation. In the in vitro comet assays for the genotoxicity in the HeLa cells, the group of Hg treatment after irradiation showed higher DNA breakage than the other groups. The tail extent moment and olive tail moment of the control group were $4.88{\pm}1.00\;and\;3.50{\pm}0.52$ while the values of the only Hg treatment group were $26.90{\pm}2.67\;and\;13.16{\pm}1.82$, respectively. The tail extent moment and olive tail moment of the only 0.001, 0.005, 0.01 Hg group were $12.24{\pm}1.82,\;8.20{\pm}2.15,\;20.30{\pm}1.30,\;12.26{\pm}0.52,\;40.65{\pm}2.94\;and \;20.38{\pm}1.49$, respectively. In the case of Hg treatment after irradiation, the tail extent moment and olive tail moment of the 0.001, 0.005, 0.01 Hg group were $56.50{\pm}3.93,\;32.69{\pm}2.48,\;62.03{\pm}5.14,\;31.56{\pm}1.97,\;72.73{\pm}3.70\;and \;39.44{\pm}3.23$, respectively. The results showed that Hg induced DNA single-strand breaks or alkali labile sites as assessed by the Comet assay. It is in good agreement with the reported results. The mercury inhibits the repair of DNA. The bacterial formamidopyrimidine-DNA glycosylase (Epg protein) recognizes and removes some oxidative DNA base modifications. Enzyme inactivation by Hg (II) may therefore be due either to interactions with rysteine residues outside the metal binding domain or to very high-affinity binding of Hg (II) which readily removes Zn (II) from the zinc finger.

• Journal of Food Hygiene and Safety
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• v.13 no.2
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• pp.87-93
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• 1998

The tannic acid (0.5 mg/ml, 1.0 mg/mi, 2.0 mg/ml) and/or cadmium (20 mg/kg) were administered by oral administration. The results were as follows: 1. There were adverse effects on the weight changes and water consumption. But, the extent of adverse changes were decreased by tannic acid administration. 2. Also, there were some significant changes in organ weight, especially relative liver weight and relative brain weight by cadmium administration, but Ta1.0 group was significant changes in relative liver weight, relative lung weight and relative thymus weight compared with control group. 3. In the hematological patterns of administered mice, there were significant changes between cadmium treated groups and control group. Hemoglobin contents, packed cell volume, platelet count and neutrophill count were significantly change compared with control group. These changes were not shown in tannic acid treated group. 4. There were serological enzymatic changes in the cadmium treated mouse. In the tannic acid treated group 0.5, 1.0, 2.0 mg/ml, ALT, AST, BUN and creatinine were recovered to the extent of control group. From the above results, the tannic acid has some possible alleviative effects of cadmium toxicity upto the 2.0 mg/ml/day of oral dose for 4 weeks. But we need further study of mechanism for toxicty alleviating action of tannic acid to the heavy metals like cadmium.