Gene/Protein Disease Symptom Drug Enzyme Compound
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 28,634 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Germinal cells isolated from Echinococcus granulosus cysts harbored in mice have been maintained in an in vitro culture system containing RPMI 1640 supplemented by 20% calf serum, and used as a model for screening anti-hydatid drugs. When the germinal cells were maintained in the medium for 6 days, the cell proliferation rate was rather high in the first four days but declined in the last two days. In screening drugs, 1.4 x 10(6) germinal cells were exposed to known effective drugs against metacestodes of E. granulosus in mice, such as mebendazole (Meb), albendazole (Alb) or praziquantel (Pra) at various concentrations. One to three days after exposure, cell counts were made daily in 3 samples of each drug concentration. The mean cell number of each group was compared with that of the control and the inhibition rate of the cell was then calculated. The results showed that the minimal effective concentrations of Meb, Alb and Pra, were 1.0 (48 h), 2.5 (24 h) and 10.0 (72 h) micrograms/ml, respectively, while the inhibition rates of the cell were 34.1, 55.7 and 18.5%. Interestingly, the in vitro effects of Meb, Alb and Pra were consistent to those obtained from the in vivo tests, ie Meb > Alb > Pra. Nevertheless, after exposure of germinal cells to Meb at 2.5 micrograms/ml for 24 h, the cells appeared in roughness, indistinction, shrunk or swelling, collapse, deformation and hole-like feature detected by light microscopy and scanning electron-microscopy, while the ultrastructure alterations of the cells noted by transmission electron-microscopy were lysis in cytoplasm, disruption or disappearance of nucleus and even darkness of the whole cell.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Screening antihydatid drugs using cultivated germinal cells of Echinococcus granulosus]. 840 69

A number of anti-cancer agents have been implicated in vascular toxicity. The effects have been attributed to direct drug toxicity towards endothelium. Little attention has been focussed on the interaction between anticancer drugs, endothelial cells and tumour secreted factors. It is well known that tumours can secrete factors such as vascular permeability factor which do affect endothelial cells and could alter their response to the vascular effects of anticancer drugs. In the present study, we have examined, in vitro, the direct effects of vinblastine (VBL), 5-fluorouracil (5-FU), melphalan (L-PAM) and the novel tubulin inhibitor combretastatin A-1 (CBS) on endothelial permeability under normal and tumour simulated conditions. Monolayers of human umbilical vein endothelial cells (HUVEC) grown on membrane filters were incubated in drug in normal growth medium or medium conditioned by the human melanoma cell line, RPMI-7951 (TCM). VBL caused a rapid increase in permeability during the first 20 minutes, which was maintained for the duration of the experiment (120 minutes). The effect was not altered by TCM or restored to control levels when VBL was replaced by drug-free medium. Similarly, CBS caused a rapid increase in permeability; however, in contrast to VBL, this increase was enhanced by TCM. The changes induced by VBL and CBS were accompanied by contraction of the endothelial F-actin cytoskeleton. Neither L-PAM nor 5-FU altered the permeability of HUVEC monolayers. This study demonstrates that certain anti-cancer agents have a direct effect on endothelial cells, leading to an increase in the permeability of endothelial monolayers. Both VBL and CBS have vascular components in their mode of action which may lead to vascular collapse and tumour necrosis.
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PMID:Effects of novel and conventional anti-cancer agents on human endothelial permeability: influence of tumour secreted factors. 906 32

In this paper, we synthesized a series of curcumin analogs and evaluated their cytotoxicity against HepG2 cells. The results exhibited that the hydroxyl group at 3,3'-position play an essential role in enhancing their anti-proliferation activity. More importantly, 3,3'-hydroxy curcumin (1b) caused apoptosis in HepG2 cells with the ROS generation, which may be mainly composed of hydroxyl radicals (HO) and H2O2. The more cytotoxic activity and ROS-generating ability of 1b may be due to the more stable in (RPMI)-1640 medium and more massive uptake than curcumin. Then the generation of ROS can disrupt the intracellular redox balance, induce lipid peroxidation, cause the collapse of the mitochondrial membrane potential and ultimately lead to apoptosis. The results not only suggest that 3,3'-hydroxy curcumin (1b) may cause HepG2 cells apoptosis through ROS-mediated pathway, but also offer an important information for design of curcumin analog.
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PMID:3,3'-OH curcumin causes apoptosis in HepG2 cells through ROS-mediated pathway. 2689 41

In this paper, we synthesized three fluorine-substituted mono-carbonyl curcumin analogs and evaluated their cytotoxicity against several cancer cells by the MTT assay. The results exhibited that all the three compounds were more active than the leading curcumin. Especially, 2,2'-F mono-carbonyl curcumin, 1a, surfaced as an important lead compound displaying almost 4-fold cytotoxicity relative to curcumin. More importantly, 1a was more stable in (RPMI)-1640 medium and more massive uptake than curcumin, which may be relationship to their cytotoxicity, apoptotic acitivity and reactive oxygen species generation. And then, the generation of reactive oxygen species can disrupt the intracellular redox balance, induce lipid peroxidation, cause the collapse of the mitochondrial membrane potential and ultimately lead to apoptosis. The results not only suggest that 2,2'-F mono-carbonyl curcumin (1a) may cause cancer cells apoptosis through reactive oxygen species-Mediated pathway, but also gives us an important information for design of mono-carbonyl curcumin analog.
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PMID:2,2'-Fluorine mono-carbonyl curcumin induce reactive oxygen species-Mediated apoptosis in Human lung cancer NCI-H460 cells. 2726 68