Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 3 de 3
Filter
Add more filters










Database
Language
Publication year range
1.
Arzneimittelforschung ; 55(8): 437-42, 2005.
Article in English | MEDLINE | ID: mdl-16149710

ABSTRACT

Buflomedil hydrochloride (CAS 55837-25-7) is a vasoactive drug with a variety of pharmacodynamic properties. Although a number of studies have been carried out to verify the beneficial effect of buflomedil in ischemic peripheral conditions, few data are reported to justify the efficacious employment of buflomedil in the treatment of cerebrovascular diseases. The aim of the present study was to better investigate the neuroprotective effect of buflomedil in normal pentobarbital-anaesthetized rats subjected to transient bilateral common artery occlusion (BCO) for 20 min. Buflomedil hydrochloride (10 mg/kg) was administered by slow intravenous infusion (90 min), starting 1 h after the onset of ischemia. The rats were sacrificed 48 h after carotid clamping. BCO caused dramatic death of hippocampal CA1 pyramidal neurons, and a significant increase in circulating levels of neuron-specific enolase (NSE) and lactate. Treatment with buflomedil attenuated ischemia-induced histological loss and damage of CA1 pyramidal cells. Furthermore, in ischemic rats, the drug restored blood lactate concentrations and serum NSE concentrations to near normal levels. These data clearly demonstrate that buflomedil is able to protect brain neurons against damage following moderate global cerebral ischemia. One could speculate that this protective effect could be related to the capability of buflomedil to improve cerebral blood flow and energy metabolism, or to a smooth muscle relaxant effect on cerebral blood vessels.


Subject(s)
Brain Ischemia/prevention & control , Pyrrolidines/therapeutic use , Vasodilator Agents/therapeutic use , Animals , Blood Glucose/metabolism , Brain Ischemia/pathology , Cell Death , Cerebrovascular Circulation/drug effects , Hippocampus/pathology , Lactic Acid/blood , Male , Phosphopyruvate Hydratase/metabolism , Pyramidal Cells/pathology , Pyruvic Acid/blood , Rats , Rats, Sprague-Dawley , Telencephalon/blood supply , Telencephalon/pathology , Tissue Fixation
2.
Toxicol Lett ; 159(3): 219-25, 2005 Dec 15.
Article in English | MEDLINE | ID: mdl-16011880

ABSTRACT

Nickel is a metal widely employed in dental alloys, and due to peculiar properties of certain nickel-based materials, it cannot be substituted with other metals in some applications. The release of nickel ions from dental alloys placed into long-term contact with mouth soft tissues is alarming because of the toxic, immunological and carcinogenic effects which have been well documented for some nickel compounds. Our study was focussed on the toxic effects induced "in vitro" on human oral epithelium by the exposure to low concentrations of nickel chloride. In view of this, we adopted a three-dimensional model of epithelial cultures, reconstituted from TR 146 cells, resembling the physiological environment of the oral cavity and useful for biocompatibility testing. The effects on cell viability, apoptosis, cellular content of reduced and oxidized glutathione (GSH and GSSG) and release of prostaglandin E(2) (PGE(2)), interleukin-8 (IL-8) and interleukin-6 (IL-6) were investigated following topical application of a NiCl(2) solution ranging from 7.6mM to 0.05 mM for 72 h. Our findings show that nickel concentrations, which do not significantly modify cell viability and inflammation mediator release, can affect the redox equilibrium and stimulate apoptosis in oral epithelium cells. Further studies are needed to demonstrate the hypothesis that the oxidative imbalance induced by nickel might be implicated in the induction of apoptosis.


Subject(s)
Epithelial Cells/drug effects , Mouth Mucosa/drug effects , Nickel/toxicity , Apoptosis/drug effects , Cell Line , Cell Survival/drug effects , Dinoprostone/metabolism , Epithelial Cells/enzymology , Glutathione/metabolism , Glutathione Disulfide/metabolism , Humans , In Situ Nick-End Labeling , Interleukins/metabolism , Models, Biological , Mouth Mucosa/cytology , Mouth Mucosa/metabolism
3.
J Agric Food Chem ; 51(17): 4903-8, 2003 Aug 13.
Article in English | MEDLINE | ID: mdl-12903943

ABSTRACT

The juice of whole fruits of Sicilian cultivars of prickly pear (Opuntia ficus indica (L.) Mill.) was investigated, and the contents of ascorbic acid, total polyphenols, and flavonoids were determined. In the juice, ferulic acid was the chief derivative of hydroxycinnamic acid and the mean concentration of total phenolic compounds was 746 microg/mL. The flavonoid fraction, analyzed by high-performance liquid chromatography-diode array detection, consisted of rutin and isorhamnetin derivatives. The juice showed antioxidant activity in the DPPH(*) test, probably due to the phenolic compounds that are effective radical scavengers. The preventive administration of the juice inhibited the ulcerogenic activity of ethanol in rat. Light microscopy observations showed an increase in mucus production and the restoration of the normal mucosal architecture. The juice is nutritionally interesting, and its dietary intake could provide protection against oxidative damage.


Subject(s)
Anti-Ulcer Agents/analysis , Antioxidants/analysis , Beverages/analysis , Fruit/chemistry , Opuntia/chemistry , Animals , Anti-Ulcer Agents/therapeutic use , Antioxidants/pharmacology , Ethanol , Flavonoids/analysis , Free Radical Scavengers/analysis , Gastric Mucosa/pathology , Male , Phenols/analysis , Rats , Rats, Wistar , Sicily , Stomach Ulcer/chemically induced , Stomach Ulcer/pathology , Stomach Ulcer/prevention & control , Ulcer
SELECTION OF CITATIONS
SEARCH DETAIL
...