5-Methoxytryptophan (5-MTP), a catabolic product of
tryptophan, can block Cox-2 overexpression in
cancer cells as well as suppress
cancer cell growth, migration and invasion. The aim of this study was to in vitro examine whether 5-MTP is able to reduce
reactive oxygen species (ROS)-induced heart
ischemia reperfusion injury and activate the cardiomyocyte's damage surveillance systems. Accordingly, rattus cardiomyocytes were treated with H2O2 as a heart
ischemia reperfusion model prior to incubation with/without 5-MTP and proteomic analysis was performed to investigate the physiologic protection of 5-MTP in H2O2-induced
ischemia reperfusion in cardiomyocyte. Our data demonstrated that 5-MTP treatment does protect cardiomyocyte in the ROS-induced
ischemia reperfusion model. 5-MTP has also been shown to significantly facilitate cell migration and wound healing via cytoskeletal regulations. Additionally, two-dimensional differential gel electrophoresis (2D-DIGE) combined matrix assisted
laser desorption ionization-time of flight mass spectrometry (MALDI-TOF/TOF MS) analysis showed that 5-MTP might modulate growth-associated
proteins, cytoskeleton regulation, redox regulation and protein folding to stimulate wound healing as well as prevent these
ischemia reperfusion-damaged cardiomyocytes from cell death through maintaining cellular redox-balance and reducing ER-stress. To our knowledge, we report for the first time the cell repair mechanism of 5-MTP against
ischemia reperfusion-damage in cardiomyocytes based on cell biology and proteomic analysis.