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Your search keyword '"Lee, Kyung-Tae"' showing total 89 results
Start Over Author "Lee, Kyung-Tae" Publisher pharmaceutical society of japan
89 results on '"Lee, Kyung-Tae"'

11. 23-Hydroxytormentic Acid and Niga-Ichgoside F1 Isolated from Rubus coreanus Attenuate Cisplatin-Induced Cytotoxicity by Reducing Oxidative Stress in Renal Epithelial LLC-PK1 Cells

Author

Kim, Yang-Hee, primary, Choi, Jung-Hye, additional, Rim, Hong-Kun, additional, Kang, Hyun-Jun, additional, Chang, Sung-Goo, additional, Park, Jae-Hoon, additional, Park, Hee-Juhn, additional, Choi, Jong-Won, additional, Kim, Soo-Dong, additional, and Lee, Kyung-Tae, additional

Published
2011
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48. Panaxydol Derived from Panax ginseng Inhibits G 1 Cell Cycle Progression in Non-small Cell Lung Cancer via Upregulation of Intracellular Ca 2+ Levels.

Author

Lee JH, Leem DG, Chung KS, Kim KT, Choi SY, and Lee KT

Subjects
Carcinoma, Non-Small-Cell Lung drug therapy, Carcinoma, Non-Small-Cell Lung metabolism, Cell Cycle drug effects, Cell Cycle Proteins metabolism, Cyclin E metabolism, Cyclin-Dependent Kinase 6 metabolism, Diynes therapeutic use, Fatty Alcohols therapeutic use, Humans, Lung Neoplasms drug therapy, Lung Neoplasms metabolism, Oncogene Proteins metabolism, Plant Extracts pharmacology, Plant Extracts therapeutic use, Retinoblastoma Protein metabolism, Up-Regulation, Calcium metabolism, Carcinoma, Non-Small-Cell Lung pathology, Diynes pharmacology, Fatty Alcohols pharmacology, G1 Phase drug effects, Lung Neoplasms pathology, Panax chemistry, Phytotherapy
Abstract

Panaxydol, a polyacetylenic compound derived from Panax ginseng has been reported to suppress the growth of cancer cells. However, the molecular mechanisms underlying cell cycle arrest by this compound in non-small cell lung cancer (NSCLC) are unknown. Our study found that panaxydol treatment induced cell cycle arrest at G 1 phase in NSCLC cells. The cell cycle arrest was accompanied by down-regulation of the protein expression of cyclin-dependent kinase (CDK) 2, CDK4, CDK6, cyclin D 1 and cyclin E, and decrease in the phosphorylation of retinoblastoma (Rb) protein. Furthermore, up-regulation of cyclin-dependent kinase inhibitor (CDKI) p21 CIP1/WAF1 and p27 KIP1 was observed in panaxydol-treated NSCLC cells. In addition, panaxydol also induced accumulation of intracellular Ca 2+ ([Ca 2+ ] i ). (Acetyloxy)methyl 2-({2-[(acetyloxy)methoxy]-2-oxoethyl}[2-(2-{2-[bis({2-[(acetyloxy)methoxy]-2-oxoethyl})amino]phenoxy}ethoxy)phenyl]amino)acetate (BAPTA-AM), the Ca 2+ chelator, attenuated not only panaxydol-induced accumulation of [Ca 2+ ] i , but also G 1 cell cycle arrest and decrease of CDK6 and cyclin D 1 protein expression level. These results demonstrated that the anti-proliferative effects of panaxydol were caused by cell cycle arrest, which is closely linked to the up-regulation of [Ca 2+ ] i and represents a promising approach for the treatment of lung cancer.

Published
2018
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49. Chikusetsusaponin IVa Methyl Ester Isolated from the Roots of Achyranthes japonica Suppresses LPS-Induced iNOS, TNF-α, IL-6, and IL-1β Expression by NF-κB and AP-1 Inactivation.

Author

Lee HJ, Shin JS, Lee WS, Shim HY, Park JM, Jang DS, and Lee KT

Subjects
Animals, Anti-Inflammatory Agents isolation & purification, Cyclooxygenase 2 genetics, Cyclooxygenase 2 metabolism, Dinoprostone metabolism, Esters isolation & purification, Interleukin-1beta genetics, Interleukin-1beta metabolism, Interleukin-6 genetics, Interleukin-6 metabolism, Lipopolysaccharides, Mice, NF-kappa B metabolism, Nitric Oxide Synthase Type II genetics, Nitric Oxide Synthase Type II metabolism, Oleanolic Acid isolation & purification, Oleanolic Acid pharmacology, Plant Roots chemistry, RAW 264.7 Cells, Saponins isolation & purification, Transcription Factor AP-1 metabolism, Tumor Necrosis Factor-alpha genetics, Tumor Necrosis Factor-alpha metabolism, Achyranthes, Anti-Inflammatory Agents pharmacology, Esters pharmacology, Oleanolic Acid analogs & derivatives, Saponins pharmacology
Abstract

We investigated the effect of chikusetsusaponin IVa (CS) and chikusetsusaponin IVa methyl ester (CS-ME) from the roots of Achyranthes japonica NAKAI on lipopolysaccharide (LPS)-induced nitric oxide (NO) and prostaglandin E2 (PGE2) production in RAW264.7 macrophages. CS-ME more potently inhibited LPS-induced NO and PGE2 production than CS. CS-ME concentration-dependently inhibited LPS-induced tumor necrosis factor (TNF)-α and interleukin (IL)-6 and IL-1β production in RAW264.7 macrophages and mouse peritoneal macrophages. Consistent with these findings, CS-ME suppressed LPS-induced expression of inducible NO synthase (iNOS) and cyclooxygenase (COX)-2 at protein level as well as iNOS, COX-2, TNF-α, IL-6, and IL-1β at mRNA level. In addition, CS-ME suppressed LPS-induced transcriptional activity of nuclear factor (NF)-κB and activator protein (AP)-1. The anti-inflammatory properties of CS-ME might result from suppression of iNOS, COX-2, TNF-α, IL-6, and IL-1β expression through downregulation of NF-κB and AP-1 in macrophages.

Published
2016
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50. Beta-D-xylopyranosyl-(1-->3)-beta-D-glucuronopyranosyl echinocystic acid isolated from the roots of Codonopsis lanceolata induces caspase-dependent apoptosis in human acute promyelocytic leukemia HL-60 cells.

Author

Lee KW, Jung HJ, Park HJ, Kim DG, Lee JY, and Lee KT

Subjects
Apoptosis physiology, Enzyme Induction drug effects, Enzyme Induction physiology, HL-60 Cells, Humans, Oleanolic Acid chemistry, Oleanolic Acid isolation & purification, Oleanolic Acid pharmacology, Plant Extracts chemistry, Plant Extracts isolation & purification, Plant Extracts pharmacology, Xylose analogs & derivatives, Xylose chemistry, Xylose isolation & purification, Xylose pharmacology, Apoptosis drug effects, Caspases biosynthesis, Codonopsis, Oleanolic Acid analogs & derivatives, Plant Roots
Abstract

We previously demonstrated that beta-D-xylopyranosyl-(1-->3)-beta-D-glucuronopyranosyl echinocystic acid (codonoposide 1c), a biologically active compound isolated from the roots of Codonopsis lanceolata, is cytotoxic to cancer cells. In the present study, we investigated the effects of codonoposide 1c on the induction of apoptosis, and its putative action pathway in HL-60 human promyelocytic leukemia cells. Codonoposide 1c-treated HL-60 cells displayed several features of apoptosis, including DNA fragmentation, formation of DNA ladders by agarose gel electrophoresis, and externalization of annexin-V targeted phosphatidylserine (PS) residues. We observed that codonoposide 1c caused activation of caspase-8, caspase-9, and caspase-3. A broad caspase inhibitor (z-VAD-fmk), caspase-8 inhibitor (z-IETD-fmk), and caspase-3 inhibitor (z-DEVD-fmk) almost completely suppressed codonoposide 1c-induced DNA fragmentation. We further found that codonoposide 1c induces mitochondrial translocation of Bid from cytosol, reduction of cytosolic Bax, and cytochrome c release from mitochondria. Interestingly, codonoposide 1c also triggered the mitochondrial release of Smac/DIABLO (second mitochondria-derived activator of caspases/direct inhibitor of apoptosis-binding protein with a low isoelectric point) into cytosol, and a reduction in X-linked inhibitor of apoptosis protein (XIAP). Taken together, our data indicate that codonoposide 1c is a potent inducer of apoptosis and facilates its activity via Bid cleavage and translocation to mitochondria, Bax reduction in cytosol, release of cytochrome c and Smac/DIABLO into the cytosol, and subsequently caspase activation, providing a potential mechanism for the cytotoxic activity of codonoposide 1c.

Published
2005
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