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Ju-Ock Kim,Hyung Soo Kim,Sun-Young Kim,Seong-Soo Jeong,Ho Jin Heo,Jeong Ho Seok,Choong Jae Lee 대한생리학회-대한약리학회 2005 The Korean Journal of Physiology & Pharmacology Vol.9 No.3
In this study, we investigated whether sphingosine-1-phosphate, furosemide, and indomethacin affect mucin release from airway goblet cells. Confluent primary hamster tracheal surface epithelial cells were metabolically radiolabeled and chased for 30 min or 24 hr in the presence of varying concentrations of the above agents to assess the effects on <SUP>3</SUP>H-mucin release. Sphingosine-1-phosphate stimulated mucin release during 30 min of treatment period in a dose-dependent manner. However, furosemide and indomethacin showed no effect on both basal and stimulated mucin release during 30 min or 24 hr of treatment period. We conclude that sphingosine-1-phosphate can affect mucin release by directly acting on airway mucin-secreting cells.
Ju Ho Kim,Sae Ock Oh,Sung Sook Jun,Jin Sup Jung,Jae Suk Woo,Yong Keun Kim,Sang Ho Lee 대한생리학회-대한약리학회 1999 The Korean Journal of Physiology & Pharmacology Vol.3 No.1
<P> It has been reported that activation of sphingomyelin pathway and nonsteroidal anti-inflammatory drugs (NSAIDS) inhibit the promotion of colon carcinoma. Ceramide, a metabolite of sphingomyelin, and indomethacin were shown to induce apoptosis in colon carcinoma cells. However, the mechanisms of ceramide- and indomethacin-induced apoptosis in the colon carcinoma cells are not clearly elucidated. Recent studys showed that indomethacin-induced apoptosis in colon cancer cells through the cyclooxygenase-independent pathways, and that may be mediated by generation of ceramide. In this study, we compared effects of ceramide and indomethacin on important modulators of apoptotic processes in HT29 cells, a human colon cancer cell line. Ceramide and indomethacin induced apoptosis dose- and time- dependently. Ceramide and indomethacin increased stress-activated protein kinase (SAPK) activity, and decreased mitogen-activated protein kinase (MAPK) activity. The expression of Bak was increased by the treatment of ceramide and indomethacin. The expression of other Bcl-2 related proteins (Mcl-1, Bcl-X<SUB>L</SUB>, Bax) which were known to be expressed in colon epithelial cells was not changed during the ceramide- and indomethacin-induced apoptosis. Our results suggest that ceramide and indomethacin share common mechanisms for induction of apoptosis in HT29 cells.
Kim, Ju-Ock,Kim, Hyung-Soo,Kim, Sun-Young,Jeong, Seong-Soo,Heo, Ho-Jin,Seok, Jeong-Ho,Lee, Choong-Jae The Korean Society of Pharmacology 2005 The Korean Journal of Physiology & Pharmacology Vol.9 No.3
In this study, we investigated whether sphingosine-1-phosphate, furosemide, and indomethacin affect mucin release from airway goblet cells. Confluent primary hamster tracheal surface epithelial cells were metabolically radiolabeled and chased for 30 min or 24 hr in the presence of varying concentrations of the above agents to assess the effects on $^3H-mucin$ release. Sphingosine-1-phosphate stimulated mucin release during 30 min of treatment period in a dose-dependent manner. However, furosemide and indomethacin showed no effect on both basal and stimulated mucin release during 30 min or 24 hr of treatment period. We conclude that sphingosine-1-phosphate can affect mucin release by directly acting on airway mucin-secreting cells.
Ju-Yeon Ban,Soon-Ock Cho,Soon-Ho Kwon,Jin-Bae Kim,Nak-Sul Song,Ki-Whan Bae,Kyung-Sik Song,Yeon-Hee Seng 한국약용작물학회 2005 한국약용작물학회지 Vol.13 No.2
Caulis Bambusae in Taenia is widely used in Korea and China due to its various pharmacological activity. The present study aims to investigate the effect of the methanol extract of Caulis Bambusae in Taenia (CB) from Phyllostachys nigra Munro var. henonis Stapf (Gramineae) on amyloid β protein (25-35) (Aβ (25-35)), a synthetic 25-35 amyloid peptide, -induced neurotoxicity using cultured rat cortical neurons. CB, over a concentration range of 10-50μg/μl, inhibited the Aβ (25-35) (10 μM)-induced neuronal cell death, as assessed by a 3-[4,5-dimethyIthiazole-2-yl]-2,5-diphenyl-tetrazolium bromide (MTT) assay and the number of apoptotic nuclei, evidenced by Hoechst 33342 staining. CB (50 μg/μl) inhibited glutamate release into medium induced by 10 μM Aβ, (25-35) which was measured by HPLC. Pretreatment of CB (50 μg/μl) inhibited 10μM Aβ (25-35)-induced elevation of cytosolic calcium concentration ([Ca2+]c), which was measured by a fluorescent dye, fluo-4 AM, and generation of reactive oxygen species. These results suggest that CB prevents Aβ (25-35)-induced neuronal ell damage in vitro.
A Study on Current Status of Pesticide Residues in Commercial Agricultural Products, 2001
Ock-Kyung Chun,Kee-Young Shin,Jib-Ho Lee,Ju-Sung Bak,Tae-Hee Cho,Tae-Rang Kim,Ouk-Hee Kim,Min-Su Chang,In-Suck Hong,Yeo-Jun Son,Sung-Ae Cho,Young-Hee Choi,Young-Ho Seo,Bok-Soon Kim,Hee-Gon Kang 한국식품과학회 2002 Food Science and Biotechnology Vol.11 No.6
Kim, Ju-Ock,Jung, Sung-Soo,Kim, Sun-Young,Kim, Tae Yun,Shin, Dae-Whan,Lee, Jae-Ho,Lee, Young-Ha The Korean Academy of Medical Sciences 2007 JOURNAL OF KOREAN MEDICAL SCIENCE Vol.22 No.suppl
<P><I>Toxoplasma gondii</I> is an obligate intracellular protozoan parasite that induces antitumor activity against certain types of cancers. However, little information is available regarding the immunologic mechanisms that regulate these effects. For this purpose, C57BL/6 mice were administered either the <I>T. gondii</I> Me49 strain orally or Lewis lung carcinoma (LLC) cells intramuscularly. Survival rates, tumor size, histopathology, and immune responses were determined for each group, and angiogenesis was evaluated by in vivo Matrigel plug assay. <I>Toxoplasma</I>-infected (TG-injected) mice survived the entire experimental period, whereas cancer cell-bearing (LLC-injected) mice died within six weeks. Mice injected with both <I>T. gondii</I> and cancer cells (TG/LLC-injected group) showed significantly increased survival rates, CD8<SUP>+</SUP> T-cell percentages, IFN-γ mRNA expression levels, serum IgG2a titers, and CTL responses as compared to the LLC-injected mice. In addition, angiogenesis in the TG/LLC-injected mice was notably inhibited. These effects in TG/LCC-injected mice were similar or were increased by the addition of an adjuvant, Quil-A. However, TG/LLC-injected mice showed decreased percentages of CD4<SUP>+</SUP> and CD8<SUP>+</SUP> T-cells, IFN-γ mRNA expression levels, and serum IgG1 and IgG2a titers as compared to TG-injected mice. Taken together, our results demonstrate that <I>T. gondii</I> infection inhibits tumor growth in the Lewis lung carcinoma mouse model through the induction of Th1 immune responses and antiangiogenic activity.</P>