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

被引:8
作者
Jiao, Yi [1 ]
Fan, Yi-Fei [1 ]
Wang, Yu-Ling [1 ]
Zhang, Jun-Yan [1 ]
Chen, Shuo [2 ]
Chen, Zhi-Wu [1 ]
机构
[1] Anhui Med Univ, Dept Pharmacol, Hefei 230032, Anhui, Peoples R China
[2] Liaoning Univ Tradit Chinese Med, Xinglin Coll, Shenyang 110167, Liaoning, Peoples R China
基金
中国国家自然科学基金;
关键词
RHO-KINASE; RHOA/RHO-KINASE; K+ CHANNELS; INHIBITION; HEART; ISCHEMIA/REPERFUSION; MYOCARDIUM; PROTEIN; INJURY; ROLES;
D O I
10.1155/2015/863531
中图分类号
R [医药、卫生];
学科分类号
10 ;
摘要
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 ROCK1 and ROCK2 protein were examined by Western blot analysis, and K+ currents were recorded by using whole-cell patch clamp technique. TFR 20 similar to 80 mg/kg markedly reduced I/R-induced myocardial infarction. TFR 3.7 similar to 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 ROCK1 and ROCK2 expressions in rat cardiomyocytes, but TFR 33.3 similar to 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 ROCK1 and ROCK2 and activation of K+ channels.
引用
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页数:10
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