• Development and Reproduction
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• v.18 no.4
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• pp.225-231
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• 2014

Autophagy is a homeostatic degradation process that is involved in tumor development and normal development. Autophagy is induced in cancer cells in response to chemotherapeutic agents, and inhibition of autophagy results in enhanced cancer cell death or survival. Chloroquine (CQ), an anti-malarial drug, is a lysosomotropic agent and is currently used as a potential anticancer agent as well as an autophagy inhibitor. Here, we evaluate the characteristics of these dual activities of CQ using human colorectal cancer cell line HCT15. The results show that CQ inhibited cell viability in dose- and time-dependent manner in the range between 20 to 80 uM, while CQ did not show any antiproliferative activity at 5 and 10 uM. Cotreatment of CQ with antitumor agent NVP-BEZ235, a dual inhibitor of PI3K/mTOR, rescued the cell viability at low concentrations meaning that CQ acted as an autophagy inhibitor, but CQ induced the lethal effect at high concentrations. Acridine orange staining revealed that CQ at high doses induced lysosomal membrane permeabilization (LMP). High doses of CQ produced cellular reactive oxygen species (ROS) and cotreatment of antioxidants, such as NAC and trolox, with high doses of CQ rescued the cell viability. These results suggest that CQ may exert its dual activities, as autophagy inhibitor or LMP inducer, in concentration-dependent manner.

• YAKHAK HOEJI
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• v.50 no.1
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• pp.58-63
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• 2006

The antioxidant enzyme (AOE) system plays an important role in the defense against oxidative stress damage. To determine whether myricetin or myricetin/taurine can exert antioxidative effects not only by modulating the AOE system directly but also by scavenging free radical, we investigated the influence of the myricetin and taurine on cell viability ROS level, activities of different antioxidant enzyme, and the expression of different antioxidant enzyme. As results, the cell viability showed inhibition of the proliferation with treatment of 'myricetin' or 'myricetin with taruine', respectively, with dose-dependent manner. Compared to control, the treatment of 'myricetin' decreased activities and gene expressions of superoxide dismutase (SOD), and glutathione peroxidase (GPx). However, combined treatment of 'myricetin with taurine' increased activities and gene expressions of the SOD, GPx, and catalase (CAT). In addition, the combined treatment of 'myricetin with taurine' somewhat decreased ROS levels, compared to the treatment of 'myricetin'. In conclusion, our study provides that the combined treatment of different antioxidants can enhance antioxidant effects.

• Toxicological Research
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• v.11 no.1
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• pp.103-108
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• 1995

Rat renal proximal tubule suspension was prepared from adult male Sprague Dawley rat (250-300g) by mechanical (non-enzymatical) method and evaluated as a pontential model for mechanistic studies and early screening of nephrotoxicity, using anionic antibiotics (cephaloridine). Cephaloridine (CPL) produced an increase in LDH release into media. This release results from decrease a proximal tubule cell viability and subsequently increase the permeability of cell viability and subsequently increase the permeability of cell membrane. Since loss of intracellular potassium and ATP into media is the sign of disruption of cell membrane, especially basolateral membrane (BLM), CPL induced proximal tubule cell compromise also appear be associated with BLM, maybe $Na^+-K^+$ ATPase. Also seen was significant depression in brush border membrane (BBM) ALP activity and no significantly increase in BBM GGT activities. The inhibition of typical anion, PAH accumulation (especially, CPL 5 mM) and cation, TEA (especially, 4hours incubation) were seen dose dependently. This is because of CPL accumulation in renal proximal tubule and increase of cytotoxicity.

• Journal of Chest Surgery
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• v.7 no.2
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• pp.145-152
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• 1974

The effect of reticuloendothelial hyperfunction on hypothermic preservation of lung was studied in dogs. In order to evaluate the viability after hemodynamic_ load in preserved isolated lung, observations were made on the rate of increase in weight, degree of edema,compliance and surface activity of lung. The results obtained as follows: l. In the group of activating of the reticuloendothelial system by injection of sodium thiosulfate intravenously before pneumonectomy and infusion of naphthionine through the pulmonary artery before hypothermic preservation of isolated lung the limit of preservation was eight hours whereas four hours in non-treated control group. 2.Therefore the method of activating of the reticuloendothelial system before and after pulmonary resection seems effective in preserving for prolonging the period of preservation of lung by means of inhibition of pulmonary edema. 3. Pulmonary surface activity is expected to be valuable as a method in evaluation of the viability of preserved lung along with compliance and rate of increase in weight of lung.

• The Journal of Korean Medicine
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• v.23 no.2
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• pp.57-69
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• 2002

Objective: The aim of this study is to investigate the effect of Injin butanol fractions with Thin Layer Chromatography on Fas-mediated Apoptosis. Method: Injin-butanol fraction separated by TLC. MIT assay, cell cycle analysis, Caspase-3 protease assay, DNA fragmentation assay and quantitative RT-PCR were performed to evaluate the effects of TLC extraction of lnjin-butanol fraction on cell viability, cell cycle progression and apoptosis. Results: Scopoletin, luteolin, apigenin and unknown powder was isolated by TLC. Fas-mediated apoptosis analysis shows that scopoletin has inhibiting function on apoptosis. Caspase- 3 protease assay analysis shows that scopoletin inhibits activity of caspase-3. Quantitative RT-PCR analysis shows that no activity on caspase-3, but apoptosis inhibition cytokine -Bcl-2- is activated, and apoptosis activating cytokine -Bax- is unactivated. Conclusion: These results show that each fraction of Injin-butanol TLC extraction, especially scopoletin, acts as a protective function on liver cell viability, and inhibitory function on apoptosis. (J Korean Oriental Moo 2002;23(2):57-69)

• Korean Journal of Acupuncture
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• v.25 no.1
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• pp.197-211
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• 2008

Objectives : We studied on anti-allergic effects of Arctii Fructus Herbal Acupuncture(AFHA) and Arctii Fructus Herbal Acupuncture Solution(AF). Methods : In vivo, Animals were herbal-acupunctured AFHA at both ST36 three times for 5 days. Then, we investigated compound 48/80-induced active systemic anaphylaxis(ASA) using ICR mice and anti-DNP IgE-induced passive cutaneous anaphylaxis(PCA) using Sprague Dawley rat. In vitro, we measured cell viability, b-hexosaminidase, IL-4 and TNF-a release from RBL-2H3 cells after treatment of AF of various concentrations. Results : In vivo, AFHA pretreatments at both ST36 inhibited compound 48/80-induced ASA. PCA was inhibited by AFHA pretreatments at both ST36. In vitro, AF treatments were not affect on cell viability and inhibited b-hexosaminidase, IL-4 and TNF-a release. Conclusions : These results suggest that AFHA and AF may be beneficial in the inhibition of allergic inflammatory response.

• Korean Journal of Acupuncture
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• v.25 no.1
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• pp.213-227
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• 2008

Objectives : We studied on anti-allergic effects of Semen Perillae Herbal Acupuncture(SPHA) and Semen Perillae Herbal Acupuncture Solution(SP). Methods : In vivo, Animals were herbal-acupunctured SPHA at both ST36 three times for 5 days. Then, we investigated compound 48/80-induced active systemic anaphylaxis (ASA) using ICR mice and anti-DNP IgE-induced passive cutaneous anaphylaxis (PCA) using Sprague Dawley rat. In vitro, we measured cell viability, b-hexosaminidase release, IL-4 and TNF-a from RBL-2H3 cells after treatment of SP of various concentrations. Results : In vivo, SPHA pretreatments at both ST36 inhibited compound 48/80-induced ASA. PCA was inhibited by SPHA pretreatments at both ST36 and optional points. In vitro, SP treatments were not affect on cell viability and inhibited b-hexosaminidase release, IL-4 and TNF-a. Conclusions : These results suggest that SPHA and SP may be beneficial in the inhibition of allergic inflammatory response.

• Journal of the Society of Cosmetic Scientists of Korea
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• v.41 no.2
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• pp.173-180
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• 2015

In the present study, antioxidant activities and tyrosinase inhibition of Perilla frutescens, Houttuynia cordata and Camellia sinensis extracts and the extract mixtures (PHC) were investigated. PHC showed 80.2% and 98.0% of free radical scavenging activity in DPPH and ABTS analysis, respectively, and 50% tyrosinase inhibition in $1000{\mu}g/mL$ concentration. HaCaT cells did not show cell toxicity in $100{\mu}g/mL$ of the PHC. Furthermore, HaCaT cell viability by co-culture with extract H. cordata was increased more than 10% compared with untreated cells. However, the cell viability was decreased in $500{\mu}g/mL$ of the extract C. sinensis and the PHC. These results suggested that about $100{\mu}g/mL$ concentration of the PHC showed proper tyrosinase inhibitory effect and antioxidant activities. The PHC could be used as multifunctional cosmeceutical agents.

• The Korea Journal of Herbology
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• v.30 no.6
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• pp.77-82
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• 2015

Objectives : This study was designed to investigate of the anti-inflammatory effects of Schisandra chinensis seed oil(SSO) on the production of pro-inflammatory substances in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages.Methods : SSO was measured the production of pro-inflammatory factor (NO, PGE2, IL-1β iNOS and, COX-2) in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages. we used the following methods : cell viability assay, Griess reagent assay, enzyme-linked immunosorbent assay, Western blotting analysis.Results : The cell viability of SSO(0∼500 μl/mL) processing group was 96.9% and the processing of SSO didn't have an effect on the cytotoxicity. The inhibitory effect of the nitric oxide (no) production of SSO(500 μg/mL, 50 μg/mL, 10 μg/mL) was each 70.3%, 37.6% and 26.5%. IL-1β production inhibition ability of SSO(500 μg/mL, 100 μg/mL) was each 49.88% and 48.8%. PGE2 production inhibition ability of SSO(500 μg/mL, 100 μg/mL) was each 49.88% and 73.1%, 70.5%. By using SSO, it experimented about iNOS protein expression inhibition ability, that is the NO production enzyme. iNOS protein expression increased in the group processing LPS independently. iNOS protein expression decreased in the group processing SSO together. The expression of the COX-2 protein decreased 89.6%, 81.8% in the group processing SSO. The significance was in the relationship with NO formation inhibition with the relationship with the PGE₂ formation inhibition and iNOS protein, it confirmed in SSO with the COX-2 protein.Conclusions : Stimulation of the RAW 264.7 cells with LPS caused an elevated production of nitric oxide (NO), IL-1β and PGE₂ which was markedly inhibited by the pretreatment with SSO without causing any cytotoxic effects. The reduced expressions of iNOS protein were consistent with the reductions in NO production in the culture media. SSO may be useful for the treatment of various inflammatory diseases.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.13
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• pp.5455-5461
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• 2014

Background: Saponins are a major active component for the traditional Chinese medicine, Rubus parvifolius L., which has shown clear antitumor activities. However, the specific effects and mechanisms of saponins of Rubus parvifolius L. (SRP) remain unclear with regard to human chronic myeloid leukemia cells. The aim of this study was to investigate inhibition of proliferation and apoptosis induction effects of SRP in K562 cells and further elucidate its regulatory mechanisms. Materials and Methods: K562 cells were treated with different concentrations of SRP and MTT assays were performed to determine cell viability. Apoptosis induction by SRP was determined with FACS and DAPI staining analysis. Western blotting was used to detect expression of apoptosis and survival related genes. Specific inhibitors were added to confirm roles of STAT3 and AMPK pathways in SRP induction of apoptosis. Results: Our results indicated that SRP exhibited obvious inhibitory effects on the growth of K562 cells, and significantly induced apoptosis. Cleavage of pro-apoptotic proteins was dramatically increased after SRP exposure. SRP treatment also increased the activities of AMPK and JNK pathways, and inhibited the phosphorylation expression level of STAT3 in K562 cells. Inhibition of the AMPK pathway blocked the activation of JNK by SRP, indicating that SRP regulated the expression of JNK dependent oon the AMPK pathway. Furthermore, inhibition of the latter significantly conferred resistance to SRP pro-apoptotic activity, suggesting involvement of the AMPK pathway in induction of apoptosis. Pretreatment with a STAT3 inhibitor also augmented SRP induced growth inhibition and cell apoptosis, further confirming roles of the STAT3 pathway after SRP treatment. Conclusions: Our results demonstrated that SRP induce cell apoptosis through AMPK activation and STAT3 inhibition in K562 cells. This suggests the possibility of further developing SRP as an alternative treatment option, or perhaps using it as adjuvant chemotherapeutic agent for chronic myeloid leukemia therapy.