Publications by authors named "Tsung-Ping Lin"

Curcumin, derived from the food flavoring spice turmeric (Curcuma longa), has been shown to exhibit anticancer activities and induce apoptosis in many types of cancer cell lines. In our previous study, curcumin was able to inhibit murine myelomonocytic leukemia WEHI-3 cells in vivo. However, there is no report addressing the cytotoxic responses and the mechanisms underlying curcumin-induced apoptotic cell death in WEHI-3 cells.

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Aims: This study was designed to examine the mechanism of relaxation induced by CIJ-3-2F, a benzyl-furoquinoline antiarrhythmic agent, in rat thoracic aorta at the tissue and cellular levels.

Main Methods: Isometric tension of rat aortic ring was measured in response to drugs. Ionic channel activities in freshly dissociated aortic vascular smooth muscle cells (VSMCs) were investigated using a whole-cell patch-clamp technique.

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JOTO1007 (ethyl 2-[N-p-chlorobenzyl-(2'-methyl)] anilino-4-oxo-4,5-dihydrofuran -3-carboxylate) has anticancer effects in human cervical cancer Ca Ski cells. However, its mechanism of action on the cell migration and invasion of human cervical cancer Ca Ski cells is not fully understood. In this study, firstly, the effects of JOTO1007 on the migration and invasion of Ca Ski cells were examined by using matrigel counting.

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Curcumin (diferuloylmethane), a phenolic compound from the plant Curcuma longa (Linn.) has been shown to exhibit antitumor activity and apoptosis in many human cancer cell lines including that of lung and liver cancer. In this study, curcumin was evaluated in BALB/c mice for its ability to inhibit pulmonary and liver adenoma formation and growth after they were orally treated with N-bis(2-hydroxypropyl)nitrosamine (DHPN).

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Human cervical cancer is potentially lethal, and therefore the development of effective and tolerable therapeutic options is vital. In the present study, the in vitro effect of the synthetized compound JOT01006 (C21H20C1NO4) on human cervical epithelioid carcinoma cell line (HeLa) was examined. The results demonstrated that JOT01006 induced morphological changes and cytotoxicity (decreased the percentage of viable cells) in a dose-dependent manner.

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Cancer chemotherapeutic agents that interfere with tubulin/microtubule function are in extensive use. Quinolone is a common structure in alkaloids and its related components exhibit several pharmacological activities. In this study, we have identified the anticancer mechanisms of 2-phenyl-4-quinolone.

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The cytotoxic effects of a new compound, ethyl 2-[N-p-chlorobenzyl-(2'-methyl)] aniline-4-oxo-4,5-dihydrofuran-3-carboxylate (JOT01007) have been tested in mouse leukemia WEHI-3 cells. In this study, the mechanisms by which JOT01007 acts on a human cervical cancer cell line (Ca Ski) to bring about an increase in the ratio of Bax/Bcl-2, reduction of the mitochondrial membrane potential (MMP), increase in the levels of cytoplasmic Ca2+, activation of caspases and fragmentation of DNA, and apoptosis were investigated. Flow cytometric analysis demonstrated that JOT01007 induced a decrease of MMP in Ca Ski cells.

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A series of 2,3,4,9-tetrahydrofuro[2,3-b]quinolin-3,4-dione and ethyl 2-(substituted aniline) -4-oxo-4,5-dihydrofuran-3-carboxylate were synthesized and evaluated for cytotoxicity on murine leukemia WEHI-3 cells. The cytotoxic effects of most compounds tested were dose-dependent and the structure-activity relationships indicated that N-substituted benzyl derivatives displayed a stronger inhibitory activity against murine leukemia WEHI-3 cells compared to non-N-substituted benzyl substituted derivatives.

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We studied the electrophysiological and antiarrhythmic actions of HA-7 [N-benzyl-7-methoxy-2,3,4,9-tetrahydrofuro[2,3-b]quinoline-3,4-dione], a furoquinoline alkaloid derivative, in guinea pig heart preparations. In the perfused whole heart model, HA-7 caused a prolongation in the basic cycle length, ventricular repolarization time, and the atrioventricular (AV) nodal Wenckebach cycle length and prolonged the refractory period of the atrium, AV node, and His-Purkinje system. The atrioventricular conduction interval was also prolonged in a frequency-dependent manner.

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