Linked Life Data

19196438

Source:http://linkedlifedata.com/resource/pubmed/id/19196438

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2009-3-25
pubmed:abstractText
Melatonin is a potent antioxidant molecule with a capacity to protect tissues from damage caused by oxidative stress. It reduces cyclosporine A (CsA)-induced cardiotoxicity; this improvement required melatonin's binding to its membrane receptors. This experimental study examined whether melatonin is a useful tool for counteracting CsA-induced apoptosis in the heart of rats. We investigated melatonin's antiapoptotic efficacy in protecting the heart and tested whether this effect was totally dependent on its binding to membrane receptors or also involved radical scavenging. In some animals, solid lipid nanoparticles (SLN) as a melatonin delivery system were used. In one group of rats, melatonin (1 mg/kg/day i.p.) was given concurrently with CsA (15 mg/kg/day s.c.; CsA-MT) for 21 days. In other animals, melatonin loaded in SLN was injected with CsA (CsA-MTSLN). Oxidative stress in heart tissue was estimated using the evaluation of lipid peroxidation and the expression of the isoform of inducible nitric oxide (iNOS). The antiapoptotic effect of melatonin was evaluated using TUNEL staining and Bcl-2 protein family expression. CsA administration produced morphological and biochemical changes in the heart of rats, while melatonin reversed the changes. In particular, since the antiapoptotic melatonin's efficacy is mainly observed when it is loaded in SLN, we suggest that MT1/MT2 pathway is not sufficient for apoptosis antagonism and the additional intracellular effects may be required. Finally, we show that, (i) melatonin significantly reduces CsA cardiotoxicity acting also on apoptotic processes, and (ii) the reduction in CsA-induced cardiotoxicity is mediated mainly by its antioxidant effect.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1600-079X
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
46
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
255-61
pubmed:meshHeading
pubmed-meshheading:19196438-Analysis of Variance, pubmed-meshheading:19196438-Animals, pubmed-meshheading:19196438-Apoptosis, pubmed-meshheading:19196438-Cyclosporine, pubmed-meshheading:19196438-Drug Carriers, pubmed-meshheading:19196438-Heart Diseases, pubmed-meshheading:19196438-Immunosuppressive Agents, pubmed-meshheading:19196438-In Situ Nick-End Labeling, pubmed-meshheading:19196438-Lipid Peroxidation, pubmed-meshheading:19196438-Lipids, pubmed-meshheading:19196438-Male, pubmed-meshheading:19196438-Malondialdehyde, pubmed-meshheading:19196438-Melatonin, pubmed-meshheading:19196438-Myocardium, pubmed-meshheading:19196438-Nanoparticles, pubmed-meshheading:19196438-Nitric Oxide Synthase Type II, pubmed-meshheading:19196438-Oxidative Stress, pubmed-meshheading:19196438-Proto-Oncogene Proteins c-bcl-2, pubmed-meshheading:19196438-Rats, pubmed-meshheading:19196438-Rats, Wistar
pubmed:year
2009
pubmed:articleTitle
Melatonin delivery in solid lipid nanoparticles: prevention of cyclosporine A induced cardiac damage.
pubmed:affiliation
Division of Human Anatomy, Department of Biomedical Sciences and Biotechnology, University of Brescia, Brescia, Italy. rezzani@med.unibs.it
pubmed:publicationType
Journal Article