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E Ragazzi

Publications and source records attributed to E Ragazzi.

94 records · Page 6Linked to original sources
PubMedDate not supplied

Receptor-mediated pathways of endothelium activity in experimental atherosclerosis.

The pharmacological characterization of endothelial receptor activity during the progression of atherosclerosis in Watanabe heritable hyperlipidemic (WHHL) rabbits was examined. The data presented show that progression of atherosclerosis affects endothelial receptor functionality in different ways. Nucleotide receptor activity is preserved for longer than that of the other endothelial receptors, i.e. muscarinic- and P2y-purinoceptors. This difference means that, in WHHL rabbit aorta, some mechanisms proposed to explain impaired endothelium-mediated relaxation in atherosclerosis must be excluded. It is therefore hypothesized that atherosclerosis in genetically hyperlipidemic animals selectively influences the receptorial arrangement of endothelium, as in other published examples of selective remodeling of receptors in arteries. Endothelial cell receptors may become a new interesting target for the development of drugs to treat atherosclerosis.

Animals↗
PubMedDate not supplied

Cytotoxicity of paclitaxel in combination with cisplatin and a new Pt-mercaptopyridine complex.

In vitro synergy has been reported for exposure to paclitaxel prior to cis-platin (cis-DDP), whereas the reverse sequence resulted in antagonism. There is no clear evidence for an intracellular origin of the schedule-dependent interaction, but several hypotheses have been proposed, such as effects at the level of DNA crosslinks, or binding to tubulin sites. The purpose of this study was to evaluate the cytotoxicity of these two drugs as single agents, in combination and in sequence, against a human colon adenocarcinoma cell line (LoVo). Moreover, we considered the new Pt-mercaptopyridine complex C/2, was like cis-platin in being able to alter DNA conformation. We have therefore studied the cytotoxic effects after single agent exposure, concomitant exposure (paclitaxel + cis-platin and paclitaxel + C/2) and sequential drugs exposure (paclitaxel-->cis-platin and cis-platin-->paclitaxel or paclitaxel-->C/2 and C/2-->paclitaxel). Our results demonstrate that the most cytotoxic effect is induced by paclitaxel and C/2 exposure both in the case of concomitant cell treatment and sequential exposure paclitaxel-->C/2.

Adenocarcinoma↗
PubMedDate not supplied

Effect of dipyridamole, 5'-(N-ethyl)-carboxamidoadenosine and 1,3-dipropyl-8-(2-amino-4-chlorophenyl)-xanthine on LOVO cell growth and morphology.

The effects of stable compounds acting on adenosine receptors, 5'-(N-ethyl)-carboxamidoadenosine (NECA: A2 and A1 adenosine receptor agonist) and 1,3-dipropyl-8-(2-amino-4-chlorophenyl)-xanthine (PACPX: selective A1 adenosine receptor antagonist) were evaluated in vitro on doxorubicin-resistant LoVo (LoVo-R) and doxorubicin-sensitive LoVo (LoVo-S) human metastatic cell lines by using the neutral red test for cell growth. The effect of dipyridamole, an adenosine uptake inhibitor, was also evaluated. The drugs had an inhibitory effect on LoVo cell growth. The association of the drugs with doxorubicin enhanced the inhibition of cell growth, particularly for NECA and PACPX on LoVo-R cells. Morphological observation with scanning electron microscopy indicated cytotoxicity of the tested compounds, alone or in association with doxorubicin both in LoVo-R or LoVo-S cells, supporting the hypothesis of inhibitory effect on tumor cell growth.

Adenosine↗