Cardioprotective Effect of 'Methylamine Irisolidone', a New Compound, in Hypoxia/Reoxygenation Injury in Cultured Rat Cardiac Myocytes

被引:5
|
作者
Mu, Yan-Ling [1 ,2 ]
Xie, Yan-Ying [2 ]
Zhou, Ling [2 ]
Zhong, Ying [2 ]
Liu, Lu [2 ]
Bai, Hong [2 ]
Wang, Yuan-Shu [2 ]
Zhang, Xiu-Mei [1 ]
机构
[1] Shandong Univ, Sch Med, Dept Pharmacol, Jinan 250012, Peoples R China
[2] Shandong Acad Med Sci, Inst Mat Med, Jinan 250062, Peoples R China
基金
中国国家自然科学基金;
关键词
CARDIOMYOCYTES; ISOFLAVONES; KAKKALIDE; DAMAGE; CELLS; METABOLITES; TECTORIDIN; PUERARIAE; ISCHEMIA; FLOS;
D O I
10.1002/cbdv.200800314
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
'Methylamine irisolidone' (=5,7-dihydroxy-6-methoxy-3-(4-methoxyphenyl)-8-[(methylamino)-methyl]-4H-[1]benzopyran-4-one), a new compound, is a structurally modified kakkalide with good water solubility. In this study, we investigated its effect on hypoxia/reoxygenation (H/R) injury in cultured rat cardiac myocytes. ne results showed that methylamine irisolidone could significantly inhibit lactate dehydrogenase (LDH) release, enhance the mitochondrial membrane potential, decrease intracellular calcium (Ca2+) associated with the attenuation of reactive oxygen species (ROS) generation, reduce contents of malondialdehyde (MDA), and increase the activity of superoxide dismutase (SOD) after H/R in a dose-dependent manner. The present study demonstrated that methylamine irisolidone can directly protect cardiomyocytes against H/R injury, primarily as a result of reduction of the intracellular Ca2+ overload coincident with an attenuation of ROS generation and ROS-mediated lipid peroxidation, which may contribute to the preservation of mitochondrion function and antioxidant against H/R injury.
引用
收藏
页码:1170 / 1177
页数:8
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