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Search Results: 1 - 10 of 9075 matches for " Eun-Ok Park "
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Sojucktang induces apoptosis via loss of mitochondrial membrane potential and caspase-3 activation in KLE human endometrial cancer cells
Yeon-Suk Oh,Hee-Young Kwon,Soo-Jin Jeong,Ki-Young Park,Sun-Young Kim,Hyo-Jung Lee,Hyo-Jeong Lee,Eun-Ok Lee,Kwang Seok Ahn,Sung-Hoon Kim
Chinese Science Bulletin , 2009, DOI: 10.1007/s11434-009-0656-7
Abstract: Sojucktang (SJT) has long been used for the treatment of endometrial diseases in Korea. However, the mechanisms responsible for the SJT-induced apoptosis in endometrial cancer cells remain unclear. In the present study, SJT was demonstrated to show cytotoxic effect and induce apoptotic cell death via mitochondrial regulation in KLE endometrial cancer cells. Linderae Radix, Glycyrrhizae Radix, Zedoariae Rhizoma, Trogopterorum Faeces and Agelicae Gigantis Radix were found to be the potent constituent herbs of SJT to significantly decrease the viability of KLE cells by a tetra zolium salt (XTT) assay. Apoptotic bodies were observed in SJT-treated KLE cells by 4′-6-diamidino-2-phenylindole (DAPI) and TdT-mediated-dUTP nick-end labeling (TUNEL) assay. SJT also increased sub-G1 DNA contents of the cell cycle undergoing apoptosis in a dose-dependent manner. Furthermore, it was observed that SJT activated caspase-3 and cleaved poly (ADP-ribose) polymerase (PARP), and decreased mitochondrial membrane potential in a dose-dependent manner. Taken together, this study shows that SJT exerts anti-tumor activity against KLE endometrial cancer cells via mitochondrial dependent apoptosis induction.
A placebo-controlled trial of Korean red ginseng extract for preventing Influenza-like illness in healthy adults
Ki-Chan Ha, Min-Gul Kim, Mi-Ra Oh, Eun-Kyung Choi, Hyang-Im Back, Sun-Young Kim, Eun-Ok Park, Dae-Young Kwon, Hye-Jeong Yang, Min-Jeong Kim, Hee-Joo Kang, Ju-Hyung Lee, Kyung-Min Choi, Soo-Wan Chae, Chang-Seop Lee
BMC Complementary and Alternative Medicine , 2012, DOI: 10.1186/1472-6882-12-10
Abstract: We will conduct a randomized, double-blind, placebo-controlled study at the onset of the influenza seasons. A total of 100 subjects 30-70 years of age will be recruited from the general populations. The subjects will be instructed to take 9 capsules per day of either the KRG extract or a placebo for a period of 3 months. The primary outcome measure is to assess the frequency of ILI onset in participated subjects. Secondary variable measures will be included severity and duration of ILI symptoms. The ILI symptoms will be scored by subjects using a 4-point scale.This study is a randomized placebo controlled trial to evaluate the efficacy of the KRG extract compared to placebo and will be provided valuable new information about the clinical and physiological effects of the KRG extract on reduction of ILI incidence including flu and upper respiratory tract infections. The study has been pragmatically designed to ensure that the study findings can be implemented into clinical practice if KRG extract can be shown to be an effective reduction strategy in ILI incidence.NCT01478009.Respiratory viruses are a major cause of influenza-like illness(ILI) symptoms in children and adults, leading to substantial morbidity and mortality each year [1-5]. The complications of ILI symptoms may occur in young children (< 1 year old) and elderly people (> 65 years old), even though ILI symptoms is most often self-limited and restrained to the upper respiratory tract [6-8]. The ILI symptoms is characterized by sudden onset of symptoms such as high fever (> 38°C) and cough in the absence of other diagnosis [9,10]. Other symptoms including myalgia, headache, chills and fatigue can only be used as optional inclusion criteria. Although it is known that rhinovirus infections cause 10% to 40% of the upper respiratory tract infection [11], with coronavirus, parainfluenza virus, adenovirus, echovirus, and coxsackievirus accounting for the remainder of cases [12,13], these viruses produce clinicall
Influence of the Chungkookjang on histamine-induced wheal and flare skin response: a randomized, double-blind, placebo controlled trial
Dae-Young Kwon, Hye-Jeong Yang, Min-Jeong Kim, Hee-Joo Kang, Hyun-Jin Kim, Ki-Chan Ha, Hyang-Im Back, Sun-Young Kim, Eun-Ok Park, Min-Gul Kim, Seok-Kwon Yun, Soo-Wan Chae, Back-Hwan Cho
BMC Complementary and Alternative Medicine , 2011, DOI: 10.1186/1472-6882-11-125
Abstract: A randomized, double-blind, placebo-controlled study in 60 healthy subjects will be carried out. Sixty volunteers (aged 20-80) who gave a written consent before entering the study will be randomized in two groups of thirty subjects each. The skin prick test with histamine solution of 10 mg/ml will be performed on the ventral forearm, 10 cm from the elbow. The subjects will be instructed to take 35 g per day of either the CKJ pills or a placebo pills for a period of 3 months. Diameters of wheal and flare will be assessing 15 minutes after performing the above-mentioned skin prick test. The primary outcome is change in wheal and flare responses. Secondary outcomes will be include change in serum histamine, immunoglobulin E, cytokines (interferon-gamma, interleukin-4, -10, and tumor necrosis factor-alpha), and eosinophil cationic protein.This study will show the potential anti-inflammatory properties of the CKJ in their skin activity when histamine is the challenging agent as occurs in the clinical situation. And the present protocol will confirm the efficacy and safety of the CKJ for allergy symptoms, suggesting more basic knowledge to conduct further randomized controlled trials (RCT). If this study will be successfully performed, the CKJ will be an alternative dietary supplemental remedy for allergy patients.NCT01402141Allergic reaction is a hypersensitive response caused by immunoglobulin E (IgE)-dependent mast cell activation. In response to IgE receptor cross-linking or other stimuli, mast cells initiate exocytosis of the contents of secretory granules. These include vasoactive amines, arachidonic acid metabolites, chemokines, and cytokines [1,2]. These pro-inflammatory mediators are responsible for activating mast cells in allergic inflammation and the hypersensitive response [3-6]. Therefore, an agent or agents capable of attenuating the production of these mediators may be used as anti-inflammatory/anti-allergic agents. Since the notion that a daily intake of
Inhibition of Connexin 26/43 and Extracellular-Regulated Kinase Protein Plays a Critical Role in Melatonin Facilitated Gap Junctional Intercellular Communication in Hydrogen Peroxide-Treated HaCaT Keratinocyte Cells
Hyo-Jung Lee,Hyo-Jeong Lee,Eun Jung Sohn,Eun-Ok Lee,Jin-Hyoung Kim,Min-Ho Lee,Sung-Hoon Kim
Evidence-Based Complementary and Alternative Medicine , 2012, DOI: 10.1155/2012/589365
Abstract: Though melatonin was known to regulate gap junctional intercellular communication (GJIC) in chick astrocytes and mouse hepatocytes, the underlying mechanism by melatonin was not elucidated in hydrogen peroxide- (H2O2-) treated HaCaT keratinocyte cells until now. In the current study, though melatonin at 2 mM and hydrogen peroxide (H2O2) at 300 μM showed weak cytotoxicity in HaCaT keratinocyte cells, melatonin significantly suppressed the formation of reactive oxygen species (ROS) in H2O2-treated HaCaT cells compared to untreated controls. Also, the scrape-loading dye-transfer assay revealed that melatonin enhances the intercellular communication by introducing Lucifer Yellow into H2O2-treated cells. Furthermore, melatonin significantly enhanced the expression of connexin 26 (Cx26) and connexin 43 (Cx43) at mRNA and protein levels, but not that of connexin 30 (Cx30) in H2O2-treated HaCaT cells. Of note, melatonin attenuated the phosphorylation of extracellular signal-regulated protein kinases (ERKs) more than p38 MAPK or JNK in H2O2-treated HaCaT cells. Conversely, ERK inhibitor PD98059 promoted the intercellular communication in H2O2-treated HaCaT cells. Furthermore, combined treatment of melatonin (200 μM) and vitamin C (10 μg/mL) significantly reduced ROS production in H2O2-treated HaCaT cells. Overall, these findings support the scientific evidences that melatonin facilitates gap junctional intercellular communication in H2O2-treated HaCaT keratinocyte cells via inhibition of connexin 26/43 and ERK as a potent chemopreventive agent.
Decursin and decursinol angelate inhibit estrogen-stimulated and estrogen-independent growth and survival of breast cancer cells
Cheng Jiang, Junming Guo, Zhe Wang, Bingxiu Xiao, Hyo-Jung Lee, Eun-Ok Lee, Sung-Hoon Kim, Junxuan Lu
Breast Cancer Research , 2007, DOI: 10.1186/bcr1790
Abstract: We treated estrogen-dependent MCF-7 and estrogen-independent MDA MB-231 human breast cancer cells with decursin and DA, and examined cell growth, apoptosis, and ERα and ERβ expression in both cell lines – and, in particular, estrogen-stimulated signaling in the MCF-7 cells. We compared these compounds with decursinol to determine their structure-activity relationship.Decursin and DA exerted growth inhibitory effects on MCF-7 cells through G1 arrest and caspase-mediated apoptosis. These compounds decreased ERα in MCF-7 cells at both mRNA and protein levels, and suppressed estrogen-stimulated genes. Decursin and the pure antiestrogen Faslodex? exerted an additive growth inhibitory effect on MCF-7 cells. In MDA MB-231 cells, these compounds induced cell-cycle arrests in the G1 and G2 phases as well as inducing apoptosis, accompanied by an increased expression of ERβ. In contrast, decursinol, which lacks the side chain of decursin and DA, did not have these cellular and molecular activities at comparable concentrations.The side chain of decursin and DA is crucial for their anti-ER signaling and breast cancer growth inhibitory activities. These data provide mechanistic rationales for validating the chemopreventive and therapeutic efficacy of decursin and its derivatives in preclinical animal models of breast cancer.Breast cancer is the most commonly diagnosed nonskin malignancy among American women, accounting for approximately 32% (211,000 cases) of all new cancer cases per year [1]. It is the second leading cause of cancer death in US women, claiming the lives of 41,000 annually. The female hormone estrogen and its classic intracellular receptor – estrogen receptor (ER) alpha – are crucial for breast development and are also causally linked to the etiology and progression of breast cancer and gynecologic cancers [2-4]. The genomic effects of estrogen are principally mediated by ERα [3], the activity of which is counter-balanced by the inhibitory ERβ [3,5-8].Estrogen, t
Reactive oxygen species involved in sulforaphane-induced STAT3 inactivation and apoptosis in DU145 prostate cancer cells
Wonil Koh,Kwang Seok Ahn,Soo-Jin Jeong,Hyo-Jung Lee,Minseok Kim,Hyo-Jeong Lee,Eun-Ok Lee,Sung-Hoon Kim
Chinese Science Bulletin , 2010, DOI: 10.1007/s11434-010-4169-1
Abstract: Signal transducer and activator of transcription factor 3 (STAT3) is a transcription factor that regulates various cellular processes such as proliferation, survival and angiogenesis in cancer cells. In the present study, we investigated the mechanisms whereby isothiocyanate sulforaphane (SFN) suppresses STAT3 activation in DU145 prostate cancer cells. SFN significantly inhibited SFN-inhibited STAT3 phosphorylation at Tyr705 as well as the deoxyribonucleic acid (DNA) binding capability in electrophoresis mobility shift assay (EMSA) in time- and concentration-dependent manner. SFN also abrogated the Janus activated kinase 2 (JAK2) phosphoraylation. In addition, SFN down-regulated STAT3-related gene products including Bcl-2, Bcl-xL, and cyclin D1 and vascular endothelial growth factor (VEGF), and inhibited the proliferation and induced apoptosis. Moreover, SFN mediated reactive oxygen species (ROS) production at the early time. Overall, these results demonstrate that ROS generation may be involved in the inhibition of JAK2/STAT3 activation and apoptosis in DU145 cells.
Paeonol Oxime Inhibits bFGF-Induced Angiogenesis and Reduces VEGF Levels in Fibrosarcoma Cells
Hyo-Jeong Lee,Seung-Ae Kim,Hyo-Jung Lee,Soo-Jin Jeong,Ihn Han,Ji Hoon Jung,Eun-Ok Lee,Shudong Zhu,Chang-Yan Chen,Sung-Hoon Kim
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0012358
Abstract: We previously reported the anti-angiogenic activity of paeonol isolated from Moutan Cortex. In the present study, we investigated the negative effect of paeonol oxime (PO, a paeonol derivative) on basic fibroblast growth factor (bFGF)-mediated angiogenesis in human umbilical vein endothelial cells (HUVECs) (including tumor angiogenesis) and pro-survival activity in HT-1080 fibrosarcoma cell line.
Retraction: Substance P and beta-endorphin mediate electro-acupuncture induced analgesia in mouse cancer pain model
Hyo-Jeong Lee, Jae-Ho Lee, Eun-Ok Lee, Hyo-Jung Lee, Kwan-Hyun Kim, Sun-Hyung Kim, Keun-Sung Lee, Hee-Jae Jung, Sung-Hoon Kim
Journal of Experimental & Clinical Cancer Research , 2009, DOI: 10.1186/1756-9966-28-137
Substance P and beta-endorphin mediate electro-acupuncture induced analgesia in mouse cancer pain model
Hyo-Jeong Lee, Jae-Ho Lee, Eun-Ok Lee, Hyo-Jung Lee, Kwan-Hyun Kim, Sun-Hyung Kim, Keun-Sung Lee, Hee-Jae Jung, Sung-Hoon Kim
Journal of Experimental & Clinical Cancer Research , 2009, DOI: 10.1186/1756-9966-28-102
Abstract: In order to produce a neuropathic cancer pain model, S-180 sarcoma cells were inoculated around the sciatic nerve of left legs of Balb/c mice. Magnetic Resonance Imaging (MRI) scanning confirmed the mass of S-180 cancer cells embedded around the sciatic nerve. Mechanical allodynia was most consistently induced in the mouse sarcoma cell line S-180 (2 × 106sarcoma cells)-treated group compared to all the other groups studied. EA stimulation (2 Hz) was administered daily to ST36 (Zusanli) of S-180 bearing mice for 30 min for 9 days after S-180 inoculation.EA treatment significantly prolonged paw withdrawal latency from 5 days after inoculation. It also shortened the cumulative lifting duration from 7 days after inoculation, compared to the tumor control. Also, the overexpression of pain peptide substance P in the dorsal horn of the spinal cord was significantly decreased in the EA-treated group compared to the tumor control on Day 9 post inoculation. Furthermore, EA treatment effectively increased the concentration of β-endorphin in blood and brain samples of the mice to a greater extent than that of the tumor control as well as the normal group. The concentration of β-endorphin for EA treatment group increased by 51.457% in the blood and 12.6% in the brain respectively, compared to the tumor control group.The findings of this study suggest that a S-180 cancer pain model is useful as a consistent and short time animal model. It also indicated that EA treatment could be used as an alternative therapeutic method for cancer pain due to a consequent decrease in substance P and increase in β-endorphin levels.Pain is a frequent problem in cancer patients. The analgesic ladder for cancer-related pain provided by the WHO involves progressing from non-opioid (e.g., acetaminophen, ibuprofen), weak opioid (e.g., codeine), and finally to strong opioid (e.g., morphine, fentanyl) intervention for pain relief [1]. Some studies have been reported that opioid switching therapy reduced
Suppression of STAT3 and HIF-1 Alpha Mediates Anti-Angiogenic Activity of Betulinic Acid in Hypoxic PC-3 Prostate Cancer Cells
Jimin Shin, Hyo-Jeong Lee, Deok-Beom Jung, Ji Hoon Jung, Hyo-Jung Lee, Eun-Ok Lee, Seok Geun Lee, Beom Sang Shim, Seung Hoon Choi, Seong Gyu Ko, Kwang Seok Ahn, Soo-Jin Jeong, Sung-Hoon Kim
PLOS ONE , 2011, DOI: 10.1371/journal.pone.0021492
Abstract: Background Signal transducer and activator of transcription 3 (STAT3) is a transcription factor that regulates various cellular processes such as cell survival, angiogenesis and proliferation. In the present study, we examined that betulinic acid (BA), a triterpene from the bark of white birch, had the inhibitory effects on hypoxia-mediated activation of STAT3 in androgen independent human prostate cancer PC-3 cells. Methodology/Principal Findings BA inhibited the protein expression and the transcriptional activities of hypoxia-inducible factor-1α (HIF-1α) under hypoxic condition. Consistently, BA blocked hypoxia-induced phosphorylation, DNA binding activity and nuclear accumulation of STAT3. In addition, BA significantly reduced cellular and secreted levels of vascular endothelial growth factor (VEGF), a critical angiogenic factor and a target gene of STAT3 induced under hypoxia. Furthermore, BA prevented in vitro capillary tube formation in human umbilical vein endothelial cells (HUVECs) maintained in conditioned medium of hypoxic PC-3 cells, implying anti-angiogenic activity of BA under hypoxic condition. Of note, chromatin immunoprecipitation (ChiP) assay revealed that BA inhibited binding of HIF-1α and STAT3 to VEGF promoter. Furthermore, silencing STAT3 using siRNA transfection effectively enhanced the reduced VEGF production induced by BA treatment under hypoxia. Conclusions/Significance Taken together, our results suggest that BA has anti-angiogenic activity by disturbing the binding of HIF-1α and STAT3 to the VEGF promoter in hypoxic PC-3 cells.
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