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Protective Effect and Mechanism of Total Flavones from Rhododendron simsii Planch Flower on Cultured Rat Cardiomyocytes with Anoxia and Reoxygenation

Many flavonoids have cardioprotection against myocardial ischemia/reperfusion (I/R) injury. Total flavones from Rhododendron simsii Planch flower (TFR) can protect myocardial ischemic injuries. However, its protective mechanism is still unknown. The present study was designed to investigate the mech...

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Detalles Bibliográficos
Autores principales: Jiao, Yi, Fan, Yi-Fei, Wang, Yu-Ling, Zhang, Jun-Yan, Chen, Shuo, Chen, Zhi-Wu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4377486/
https://www.ncbi.nlm.nih.gov/pubmed/25861370
http://dx.doi.org/10.1155/2015/863531
Descripción
Sumario:Many flavonoids have cardioprotection against myocardial ischemia/reperfusion (I/R) injury. Total flavones from Rhododendron simsii Planch flower (TFR) can protect myocardial ischemic injuries. However, its protective mechanism is still unknown. The present study was designed to investigate the mechanism of TFR on myocardial I/R and anoxia/reoxygenation (A/R) injuries. Rat model of myocardial I/R injury was made, and myocardial infarction was determined. A/R injury was induced in cultured rat cardiomyocytes; cellular damage was evaluated by measuring cell viability, LDH and cTnT releases, and MDA content. Expressions of ROCK(1) and ROCK(2) protein were examined by Western blot analysis, and K(+) currents were recorded by using whole-cell patch clamp technique. TFR 20~80 mg/kg markedly reduced I/R-induced myocardial infarction. TFR 3.7~300 mg/L significantly inhibited A/R-induced reduction of cell viability, LDH and cTnT releases, and MDA production. Exposure to A/R significantly increased ROCK(1) and ROCK(2) expressions in rat cardiomyocytes, but TFR 33.3~300 mg/L obviously inhibited this increase. 300 mg/L TFR significantly augmented inward rectifier K(+) current and other K(+) currents in rat cardiomyocytes. These results indicate that TFR has a protective effect on rat cardiomyocytes A/R damage, and the protective mechanism may be engaged with the inhibition of ROCK(1) and ROCK(2) and activation of K(+) channels.