Cardioprotective effect of 2,3-dehydrosilybin preconditioning in isolated rat heart
Jazyk angličtina Země Nizozemsko Médium print-electronic
Typ dokumentu časopisecké články
PubMed
30385403
DOI
10.1016/j.fitote.2018.10.028
PII: S0367-326X(18)31628-9
Knihovny.cz E-zdroje
- Klíčová slova
- Dehydrosilybin, Ischemia-reperfusion injury, Preconditioning, Signalosomes, Silymarin,
- MeSH
- infarkt myokardu farmakoterapie MeSH
- kardiotonika farmakologie MeSH
- krysa rodu Rattus MeSH
- potkani Wistar MeSH
- reperfuzní poškození farmakoterapie MeSH
- silymarin farmakologie MeSH
- srdce účinky léků MeSH
- techniky in vitro MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- dehydrosilybin MeSH Prohlížeč
- kardiotonika MeSH
- silymarin MeSH
2,3-dehydrosilybin (DHS) is a minor component of silymarin, Silybum marianum seed extract, used in some dietary supplements. One of the most promising activities of this compound is its anticancer and cardioprotective activity that results, at least partially, from its cytoprotective, antioxidant, and chemopreventive properties. The present study investigated the cardioprotective effects of DHS in myocardial ischemia and reperfusion injury in rats. Isolated hearts were perfused by the Langendorff technique with low dose DHS (100 nM) prior to 30 min of ischemia induced by coronary artery occlusion. After 60 min of coronary reperfusion infarct size was determined by triphenyltetrazolium staining, while lactatedehydrogenase activity was evaluated in perfusate samples collected at several timepoints during the entire perfusion procedure. Signalosomes were isolated from a heart tissue after reperfusion and involved signalling proteins were detected. DHS reduced the extent of infarction compared with untreated control hearts at low concentration; infarct size as proportion of ischemic risk zone was 7.47 ± 3.1% for DHS versus 75.3 ± 4.8% for ischemia. This protective effect was comparable to infarct limitation induced by ischemic preconditioning (22.3 ± 4.5%). Selective inhibition of Src-family kinases with PP2 (4-Amino-3-(4-chlorophenyl)-1-(t-butyl)-1H-pyrazolo[3,4-d]pyrimidine) abrogated the protection afforded by DHS. This study provides experimental evidence that DHS can mediate Src-kinase-dependent cardioprotection against myocardial damage produced by ischemia/reperfusion injury.
Department of Physiology Faculty of Medicine and Dentistry Palacký University Olomouc Czech Republic
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