Major research interests in my lab including

1] the study of the molecular and electrophysiological mechanism responsible for the generation of cardiac arrhythmia, ischemia and ischemia/reperfusion injury.

2] the study of the molecular and pathophysiological mechanism underlying the generation of cardiomyopathy and heart failure,

3] search for agents with antiarrhythmic and cardioprotective activities in animals subjected to coronary artery occlusion and reperfusion.

4] search for agents with antidiabetic activities and cardiac protective activity in type 1 and type 2 diabetic animals.

5] search for agents which can prevent organ failure and increase survival of septic animals.

During the studies of various agents in various animal models, isolated organ, tissue or cultured cells, some agents were found to have antidiabetic activity and exert cardiac protective activity and increase aurvivals in animals subjected to coronary artery occlusion/reperfusion on LPS-induced endotoxemia. Among them, some families of compounds were patented by Japan, U.S., Taiwan, and China government. Among them, patents for two group of compounds have been authorized to local pharmaceutical company for development as therapeutic agents in diabetic and cardiovascular diseases. In addition to search of cardioprotective agents in diseased animal models, the cellular mechanisms responsible for drug-induced or ischemia and/or reperfused induced cardiac injuries or cardiac protection were examined in cultured cardiac cell or isolated cardiac cells. We found that overproduction of ROS is a major cause of cell death in I/R injury. The ROS-induced activation of transient receptor potential M2 (TRPM2) channels may induce cellular and mitochondria Na+ and Ca+ overload and resulting in cytochrome c release apoptosis. The ROS induced cellular damage and mitochondrial can be prevented by some of the agents which exerted cardioprotective activity in diseased animals.

Publications:

1] Antifibrotic effects of KS370G, a caffeamide derivative, in renal ischemia-reperfusion injured mice and renal tubular epithelial cells. Sci Rep, 4:5814. 2014.   [Abstract]

2] Caffeic acid phenethyl amide ameliorates ischemia/reperfusion injury and cardiac dysfunction in streptozotocin-induced diabetic rats. Cardiovasc Diabetol, 13:98. 2014.  [Abstract]

3] Hypoglycemic action of borapetoside A from the plant Tinospora crispa in mice. Phytomedicine, 20:667-675. 2013.  [Abstract]

4] DPP4 deficiency exerts protective effect against H2O2 induced oxidative stress in isolated cardiomyocytes. PLoS One, 8:e54518. 2013.  [Abstract]

5] Thaliporphine preserves cardiac function of endotoxemic rabbits by both directly and indirectly attenuating NFκB signaling pathway. PLoS One. 7(6):e39174.2012. [Abstract]

1] the study of the molecular and electrophysiological mechanism responsible for the generation of Pharmacological studies of the cardiovascular effects (National Science Council, The National   Science and Technology Program for Biotechnology and Pharmaceuticals, NSC 97-2323-B-007)

2] the study of the molecular and electrophysiological mechanism responsible for the generation of Drug discovery for metabolic disorder diseases (National Science Council, The National Science and Technology Program for Biotechnology and Pharmaceuticals, NSC 96-3114-P-002-002-Y)

3]  Preclinical study of NTU-A (National Science Council, The National Science and Technology Program for Biotechnology and Pharmaceuticals, NSC 96-3114-P-002-002-Y)

4]  Investigation of the cardiac protective agents in endotoxaemia-induced myocardial depression (3/3) (National Science Council, NSC 96-2320-B-002-028-)

1] Dagan 8900 patch clamp amplifier: measurement of ionic currents

2] HSE-force transducer coupled with Axonclamp 2B amplifier: measurement of electromechanical response of cardiac tissues

3] Power Lab acquisition system: recording of biological signals