• The Korean Journal of Food And Nutrition
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• v.14 no.4
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• pp.329-332
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• 2001

The antimutagenic activity of resveratrol on the mutagenicity induced by Trp P-1 (3-amino-1,4-dime-thyl-5H-pyrido{4,3-b}indole) was studied using the Ames test with Salmonella typhimurium TA98 and 100. Trp P-1 showed strong mutagenecity in S. typhimurium TA98, but was higly decreased mutagenecity in S. typhimurium TA100. This result suggests that the mutagenecity of Trp P-1 can be mainly induced by the DNA lesions causing frame shift. Resveratrol itself did not show antibacterial effect upon 300 $\mu\textrm{g}$/assay. Resveratrol showed the strongest inhibitory effect with dose dependent manner on the mutagenicity induced by Trp P-1. The inhibition rates of resveratrol at concentration of 2, 10, 25, 50, 100, 300 $\mu\textrm{g}$/assay were 13%, 37%, 52%, 65%, 81%, 89%, respectively.

• The Korean Journal of Zoology
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• v.37 no.3
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• pp.377-384
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• 1994

The present study examines the inhibitow effect of progesterone (P) on luteinizing hormone $(LH)\beta$ subunit gene expression in anterior pituitary of ovariectomized, estradiol-treated adult rats. A single injection of P (1mg) further decreased the estradiol-Induced decrease in $LH\beta$ mRNA levels in ovariectomTzed rats in a time-dependent manner. p suppressed UIP mRNA levels at lower doses (0.1 and 1mg), but increased $LH\beta$ mRNA levels 81 a high dose (toms). The inhibitor action of P on $Uf\beta$ mRNA was restored when Ru486, a P receptor antagonist, was administered 1h before P treatment. These data clearly indicate that P inhibits gene expression of $LH\beta$ in the rift pituitary in a swersic manner with estrogen.

• Biomolecules & Therapeutics
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• v.22 no.1
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• pp.68-72
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• 2014

When chemotherapy is administered during pregnancy, it is important to consider the fetus chemotherapy exposure, because it may lead to fetal consequences. Paclitaxel has become widely used in the metastatic and adjuvant settings for woman with cancer including breast and ovarian cancer. Therefore, we attempted to clarify the transport mechanisms of paclitaxel through blood-placenta barrier using rat conditionally immortalized syncytiotrophoblast cell lines (TR-TBTs). The uptake of paclitaxel was time- and temperature-dependent. Paclitaxel was eliminated about 50% from the cells within 30 min. The uptake of paclitaxel was saturable with $K_m$ of $168{\mu}M$ and $371{\mu}M$ in TR-TBT 18d-1 and TR-TBT 18d-2, respectively. [$^3H$]Paclitaxel uptake was markedly inhibited by cyclosporine and verapamil, well-known substrates of P-glycoprotein (P-gp) transporter. However, several MRP substrates and organic anions had no effect on [$^3H$]paclitaxel uptake in TR-TBT cells. These results suggest that P-gp may be involved in paclitaxel transport at the placenta. TR-TBT cells expressed mRNA of P-gp. These findings are important for therapy of breast and ovarian cancer of pregnant women, and should be useful data in elucidating teratogenicity of paclitaxel during pregnancy.

• ETRI Journal
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• v.16 no.3
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• pp.1-10
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• 1994

Undoped GaAs has been successfully grown by chemical beam epitaxy (CBE) via surface decomposition process using arsine $(AsH_3)$ and trimethylgallium (TMG). Three distinct regions of temperature-dependent growth rates were identified in the range of temperatures from 570 to $690^{\circ}C$. The growth rates were found strongly dependent on the V/III ratio between 5 and 30. The growth rate at low V/III ratio seems to be determined by arsenic produced on the surface, whereas at high V/III ratio it shows dependence on the adsorption of TMG. Hall measurement and photoluminescence (PL) analysis show that the films are all p-type and that carbon impurities are primarily responsible for the background doping. Carbon concentrations have been found to be reduced by two orders of magnitude as compared to those of epilayers grown by CBE which employs TMG and arsenic obtained from precracked $AsH_3$ in a high temperature cell. It was also found that hydrogen atoms dissociated from unprecracked $AsH_3$ play an important role in removing hydrocarbon-containing species resulting in a significant reduction of car-bon impurities.

• Proceedings of the Korean Society of Applied Pharmacology
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• 1996.04a
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• pp.219-219
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• 1996

Mucin release from hamster tracheal surface epithelial(HTSE) cells can be stimulated by extracellular ATP via activation of P$_2$ purinoceptors located on the cell surface which appears to be coupled to phospholipase C via G proteins. However, our preliminary data indicate that the ATP-induced mucin release involves, in part, activation of PKC, but not an increase in the intracellular Ca++ level, suggesting the presence of another pathway which is separate from the PLC-PKC pathway, In this study, we intended to confirm the previous observation and subsequently identify an additional mechanism. Confluent HTSE cells were metabolically labeled with either $^3$H-glucosamine or $^3$H-arachidonic acid(AA), and release of either $^3$H-mucin or $^3$H-AA was quantified following various treatments. $^3$H-mucin was assayed using the sepharose CL-4B gel-filtration method, whereas $^3$H-AA liberation was measured by counting $^3$H-radioactivity in the chase medium. We found that: (1)Desensitization of PKC by pretreatment with PMA completely abolished the mucin releasing effect of PMA but partially inhibited the ATP-induced mucin release; (2) ATP increases release of $^3$H-AA in a dose-dependent fashion; (3) mepacrine, an inhibitor of PLA$_2$, attenuates ATP-induced mucin release in a dose-dependent fashion. These results confirm our previous notion that the PLC-PKC pathway is responsible, in part, for ATP-induced mucin release. Furthermore, activation of PLA$_2$ appears to be an additional pathway which is involved in ATP-induced mucin release.

• Biomedical Science Letters
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• v.8 no.4
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• pp.251-256
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• 2002

This study was undertaken to determine the underlying mechanisms of reactive oxygen species-induced cell injury in renal epithelial cells and whether there is a difference in the role of lipid peroxidation between freshly isolated renal cells and cultured renal cells. Rabbit renal cortical slices were used as a model of freshly isolated cells and opossum kidney (OK) cells as a model of cultured cells. Cell injury was estimated by measuring lactate dehydrogenase (LDH) release in renal cortical slices and frypan blue exclusion in OK cells. $H_2O$$_2$ was used as a drug model of reactive oxygen species. $H_2O$$_2$ induced cell injury in a dose-dependent manner in both cell types. However, renal cortical slices were resistant to $H_2O$$_2$ approximately 50-fold than OK cells. $H_2O$$_2$-induced cell injury was prevented by thiols (glutathione and dithiothreitol) and iron chelators (deferoxamine and phenanthroline) in both cell types. $H_2O$$_2$-induced cell injury in renal cortical slices was completely prevented by antioxidants N,N-diphenyl-p -phenylenediamine and Trolox, but the cell injury was not affected by these antioxidants in OK cells. $H_2O$$_2$ increased lipid peroxidation in both cell types, which was completely inhibited by the antioxidants. These results suggest that $H_2O$$_2$ induces cell injury through a lipid peroxidation-dependent mechanism in freshly isolated renal cells, but via a mechanism independent of lipid peronidation in cultured cells.

• Journal of Microbiology and Biotechnology
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• v.27 no.3
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• pp.584-590
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• 2017

Ginkgo biloba extract (EGb 761) has been widely used clinically to reduce myocardial ischemia reperfusion injury (MIRI). Microvascular endothelial cells (MVECs) may be a proper cellular model in vitro for the effect and mechanism study against MIRI. However, the protective effect of EGb 761 on MVECs resisting hypoxia/reoxygenation (H/R) injury is little reported. In this study, H/R-injured MVECs were treated with EGb 761, and then the cell viability, apoptosis, ROS production, SOD activity, caspase-3 activity, and protein level of ATM, ${\gamma}$-H2AX, p53, and Bax were measured. ATM siRNA was transfected to study the changes of protein in the ATM pathway. EGb 761 presented protective effect on H/R-injured MVECs, with decreasing cell death, apoptosis, and ROS, and elevated SOD activity. Next, EGb 761 could inhibit H/R-induced ATM, ${\gamma}$-H2AX, p53, and Bax in a dose-dependent manner. Moreover, ATM siRNA also could inhibit H/R-induced ATM, ${\gamma}$-H2AX, p53, and Bax. Overall, these findings verify that EGb 761 protects cardiac MVECs from H/R injury, and for the first time, illustrate the influence on the ATM pathway and apoptosis by EGb 761 via dampening ROS.

• Journal of The Korean Society of Integrative Medicine
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• v.8 no.4
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• pp.163-169
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• 2020

Purpose : This study aimed to investigate the anti-allergic effect of Persicaria perfoliata water extract (PPWE) on IgE stimulated rat basophilic leukemia (RBL-2H3) cell line. Methods : P. perfoliata (L.) H. Gross has been used in traditional medicine as an anti-allergic agent, antipyretic, and diuretic and for respiratory disorders. To analyze the anti-allergic activity of PPWE, release of β-hexosaminidase in RBL-2H3 cells was estimated by enzyme linked immunosorbant assay (ELISA). Also, the cytotoxic effect of PPWE was identified by WST assay, and nuclear factor (NF)-κB and its upstream signaling molecules were assessed by western blot analysis. Results : PPWE treatment significantly attenuated β-hexosaminidase release in a dose dependent manner without any cytotoxicity. PPWE inhibited β-hexosaminidase activity by 38.4±1.2, 36.6±0.6, 32.5±2.2 and 26.5±1.2 at 500, 250, 100, and 50 ㎍/㎖ of PPWE, respectively, compared with the control group. In addition, an analysis of the expression level of NF-κB, an inflammation transcription factor, in RBL-2H3 cells upon IgE stimulation provided reults consistent with the results of β-hexosaminidase release. The phosphorylated status of upstream signaling molecules for transcription factor, mitogen activated protein kinases (MAPKs), was also analyzed. The results showed that PPWE treatment dose-dependently inhibited phosphorylation of extracellular regulatory kinase (ERK) and c-Jun N-terminal kinase (JNK). These results show that PPWE had a strong IgE-mediated degranulation inhibitory effect on RBL-2H3 cells. Conclusion : P. perfoliata ameliorated IgE-mediated allergic reaction via the modulation of MAPK and NF-κB signaling pathway in RBL-2H3 cells. These results indicate that P. perfoliata could be a potential candidate for a treatment strategy against various allergic disorders.

• The Korea Journal of Herbology
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• v.28 no.6
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• pp.155-160
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• 2013

Objectives : Gastric cancer is a leading cause of cancer-related deaths, worldwide. Houttuynia cordata Thunberg (H. cordata) has been used as a medicinal plants and it has an anti-cancer activity in human colorectal cancer and leukemic cancer. However, the potential anti-cancer activity and mechanisms of H. cordata for human gastric cancer cells have not been tested so far. Thus, this study examined the biological effects of H. cordata on the human gastric cancer cell line SNU-1 and AGS. Methods : Inhibition of cell proliferation and cell cycle by H. cordata was carried out by MTT assay and Muse cell cycle analysis and the expressions of protein associated with apoptosis and cell cycle regulation were investigated with Western blot analysis. Results : In MTT assay, the proliferation of SNU-1 and AGS cells was significantly inhibited by H. cordata in a time and dose dependent manner, Inhibition of cell proliferation by H. cordata was in part associated with apoptotic cell death, as shown by changes in the expression ratio of Bax to Bcl-2 by H. cordata. Also, H. cordata regulated the expression of cell cycle regulatory proteins such as pRb, cyclin D1, cyclin E, CDK4, CDK2, p21 and p15. Conclusion : The antiproliferative effect of H. cordata on SNU-1 and AGS gastric cancer cells revealed in this study suggests that H. cordata has intriguing potential as a chemopreventive or chemotherapeutic agent.

• The Korean Journal of Physiology and Pharmacology
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• v.21 no.5
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• pp.495-507
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• 2017

The effect of clonidine administered intrathecally (i.t.) on the mortality and the blood glucose level induced by sepsis was examined in mice. To produce sepsis, the mixture of D-galactosamine (GaLN; 0.6 g/10 ml)/lipopolysaccharide (LPS; $27{\mu}g/27{\mu}l$) was treated intraperitoneally (i.p.). The i.t. pretreatment with clonidine ($5{\mu}g/5{\mu}l$) increased the blood glucose level and attenuated mortality induced by sepsis in a dose-dependent manner. The i.t. post-treatment with clonidine up to 3 h caused an elevation of the blood glucose level and protected sepsis-induced mortality, whereas clonidine post-treated at 6, 9, or 12 h did not affect. The pre-treatment with oral D-glucose for 30 min prior to i.t. post-treatment (6 h) with clonidine did not rescue sepsis-induced mortality. In addition, i.t. pretreatment with pertussis toxin (PTX) reduced clonidine-induced protection against mortality and clonidine-induced hyperglycemia, suggesting that protective effect against sepsis-induced mortality seems to be mediated via activating PTX-sensitive G-proteins in the spinal cord. Moreover, pretreatment with clonidine attenuated the plasma tumor necrosis factor ${\alpha}$ ($TNF-{\alpha}$) induced by sepsis. Clonidine administered i.t. or i.p. increased $p-AMPK{\alpha}1$ and $p-AMPK{\alpha}2$, but decreased p-Tyk2 and p-mTOR levels in both control and sepsis groups, suggesting that the up-regulations of $p-AMPK{\alpha}1$ and $p-AMPK{\alpha}2$, or down-regulations of p-mTOR and p-Tyk2 may play critical roles for the protective effect of clonidine against sepsis-induced mortality.