Quercetin Improves Postischemic Recovery of Heart Function in Doxorubicin-Treated Rats and Prevents Doxorubicin-Induced Matrix Metalloproteinase-2 Activation and Apoptosis Induction

Autor: Ľudmila Okruhlicová, Mária Fogarassyová, Narcisa Tribulova, Ima Dovinova, Monika Bartekova, Miroslav Barancik, Petra Šimončíková, Monika Ivanova
Jazyk: angličtina
Rok vydání: 2015
Předmět:
Male
Apoptosis
Blood Pressure
Matrix metalloproteinase
quercetin
lcsh:Chemistry
chemistry.chemical_compound
polycyclic compounds
Medicine
Myocytes
Cardiac
lcsh:QH301-705.5
Spectroscopy
biology
matrix metalloproteinases
General Medicine
Computer Science Applications
Up-Regulation
Reperfusion Injury
Matrix Metalloproteinase 2
Quercetin
medicine.drug
musculoskeletal diseases
medicine.medical_specialty
ischemic tolerance
Heart Ventricles
Ischemia
heart
doxorubicin
Catalysis
Article
Inorganic Chemistry
Superoxide dismutase
Downregulation and upregulation
Internal medicine
Animals
cell signaling
Doxorubicin
Physical and Theoretical Chemistry
Rats
Wistar
Molecular Biology
business.industry
Superoxide Dismutase
Myocardium
Organic Chemistry
medicine.disease
Rats
carbohydrates (lipids)
body regions
Endocrinology
chemistry
lcsh:Biology (General)
lcsh:QD1-999
Connexin 43
biology.protein
business
Reperfusion injury
Proto-Oncogene Proteins c-akt
Zdroj: International Journal of Molecular Sciences, Vol 16, Iss 4, Pp 8168-8185 (2015)
International Journal of Molecular Sciences
Volume 16
Issue 4
Pages 8168-8185
ISSN: 1422-0067
Popis: Quercetin (QCT) is flavonoid that possesses various biological functions including anti-oxidative and radical-scavenging activities. Moreover, QCT exerts some preventive actions in treatment of cardiovascular diseases. The aim of present study was to explore effects of prolonged administration of QCT on changes induced by repeated application of doxorubicin (DOX) in rat hearts. We focused on the ultrastructure of myocardium, matrix metalloproteinases (MMPs), biometric parameters, and apoptosis induction. Our aim was also to examine effects of QCT on ischemic tolerance in hearts exposed to chronic effects of DOX, and to determine possible mechanisms underlying effects of QCT. Our results showed that QCT prevented several negative chronic effects of DOX: (I) reversed DOX-induced blood pressure increase
(II) mediated improvement of deleterious effects of DOX on ultrastructure of left ventricle
(III) prevented DOX-induced effects on tissue MMP-2 activation
and (iv) reversed effects of DOX on apoptosis induction and superoxide dismutase inhibition. Moreover, we showed that rat hearts exposed to effects of QCT were more resistant to ischemia/reperfusion injury. Effects of QCT on modulation of ischemic tolerance were linked to Akt kinase activation and connexin-43 up-regulation. Taken together, these results demonstrate that prolonged treatment with QCT prevented negative chronic effects of DOX on blood pressure, cellular damage, MMP-2 activation, and apoptosis induction. Moreover, QCT influenced myocardial responses to acute ischemic stress. These facts bring new insights into mechanisms of QCT action on rat hearts exposed to the chronic effects of DOX.
Databáze: OpenAIRE
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