Isosteviol Sensitizes sarcKATP Channels towards Pinacidil and Potentiates Mitochondrial Uncoupling of Diazoxide in Guinea Pig Ventricular Myocytes

被引:8
作者
Fan, Zhuo [1 ,2 ,3 ]
Wen, Ting [1 ,2 ]
Chen, Yaoxu [1 ,2 ]
Huang, Lijie [1 ,2 ]
Lin, Wei [1 ,2 ]
Yin, Chunxia [1 ,2 ]
Tan, Wen [1 ,2 ,3 ]
机构
[1] S China Univ Technol, Sch Biosci & Bioengn, Guangzhou 510006, Guangdong, Peoples R China
[2] S China Univ Technol, Preincubator Innovat Drugs & Med, Guangzhou 510006, Guangdong, Peoples R China
[3] S China Univ Technol, Guangdong Prov Key Lab Fermentat & Enzyme Engn, Guangzhou 510006, Guangdong, Peoples R China
基金
中国国家自然科学基金;
关键词
K-ATP CHANNELS; ISCHEMIA-REPERFUSION; POTASSIUM CHANNELS; SULFONYLUREA RECEPTOR; ADENOSINE; STEVIOSIDE; HEART; PROTEIN; MYOCARDIUM; OPENER;
D O I
10.1155/2016/6362812
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
K-ATP channel is an important mediator or factor in physiological and pathological metabolic pathway. Activation of K-ATP channel has been identified to be a critical step in the cardioprotective mechanism against IR injury. On the other hand, desensitization of the channel to its opener or themetabolic ligand ATP in pathological conditions, like cardiac hypertrophy, would decrease the adaption of myocardium to metabolic stress and is a disadvantage for drug therapy. Isosteviol, obtained by acid hydrolysis of stevioside, has been demonstrated to play a cardioprotective role against diseases of cardiovascular system, like anti-IR injury, antihypertension, antihyperglycemia, and so forth. The present study investigated the effect of isosteviol (STV) on sarcK(ATP) channel current induced by pinacidil and mitochondrial flavoprotein oxidation induced by diazoxide. Our results showed that preincubating cells with STV not only increased the current amplitude and activating rate of sarcK(ATP) channels induced by pinacidil but also potentiated diazoxide-elicited oxidation of flavoprotein in mitochondria.
引用
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页数:13
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