Cardioprotective effect of 2,3-dehydrosilybin preconditioning in isolated rat heart
Language English Country Netherlands Media print-electronic
Document type Journal Article
PubMed
30385403
DOI
10.1016/j.fitote.2018.10.028
PII: S0367-326X(18)31628-9
Knihovny.cz E-resources
- Keywords
- Dehydrosilybin, Ischemia-reperfusion injury, Preconditioning, Signalosomes, Silymarin,
- MeSH
- Myocardial Infarction drug therapy MeSH
- Cardiotonic Agents pharmacology MeSH
- Rats MeSH
- Rats, Wistar MeSH
- Reperfusion Injury drug therapy MeSH
- Silymarin pharmacology MeSH
- Heart drug effects MeSH
- In Vitro Techniques MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Names of Substances
- dehydrosilybin MeSH Browser
- Cardiotonic Agents 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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