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Oxidative Medicine and Cellular Longevity
Volume 2016 (2016), Article ID 6362812, 13 pages
Research Article

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

Zhuo Fan,1,2,3 Ting Wen,1,2 Yaoxu Chen,1,2 Lijie Huang,1,2 Wei Lin,1,2 Chunxia Yin,1,2 and Wen Tan1,2,3

1School of Bioscience and Bioengineering, South China University of Technology, Guangzhou 510006, China
2Pre-Incubator for Innovative Drugs and Medicine, South China University of Technology, Guangzhou 510006, China
3Guangdong Provincial Key Laboratory of Fermentation and Enzyme Engineering, South China University of Technology, Guangzhou 510006, China

Received 4 November 2015; Revised 29 December 2015; Accepted 30 December 2015

Academic Editor: Rajesh Mohanraj

Copyright © 2016 Zhuo Fan et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


channel is an important mediator or factor in physiological and pathological metabolic pathway. Activation of 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 the metabolic 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 sarc 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 sarc channels induced by pinacidil but also potentiated diazoxide-elicited oxidation of flavoprotein in mitochondria.