A frog antioxidant peptide protects against myocardial ischemia reperfusion injury in rats

Excessive reactive oxygen species (ROS) induced by myocardial ischemia reperfusion (IR) injury exert detrimental effects on cardiomyocytes. Antioxidant peptides can scavenge free radicals such as 2,2'-azinobis(3-ethylbenzothiazoline-6-sulfonic acid) (ABTS(+)), 2,2-diphenyl-1-picrylhydrazyl (DPPH) and nitic oxide (NO) in vitro, but little is known about their functions in vivo. Here, we evaluated the effects of an antioxidant peptide (antioxidant-RL) used at the beginning of reperfusion on myocardial IR injury. We performed 2, 3, 5-triphenyltetrazolium chloride staining (TTC) to determine myocardial infarct size. Creatine kinase isoenzyme-MB (CK-MB), cardiac troponin-T (CTnT), tumor necrosis factor-alpha (TNF-alpha), and interleukin-6 (IL-6) levels were determined with enzyme-linked immunosorbent assays (ELISAs). The levels of ROS were measured with a fluorometric Intracellular ROS kit. The expression levels of apoptosis-related proteins in cardiomyocytes were detected by western blotting. Antioxidant-RL (10 mg/kg) reduced the infarct size and levels of CK-MB and CTnT in rats. The levels of TNF-alpha and IL-6 also decreased. Furthermore, ROS levels were ameliorated and the expression of apoptosis-related proteins in myocytes was down-regulated by antioxidant-RL (100 mu g/mL). Antioxidant-RL exerted protective effects on myocardial IR injury by scavenging excessive ROS, suppressing inflammatory factors, and inhibiting cardiomyocytes apoptosis. Thus, antioxidant-RL may serve as a potent candidate for the treatment of IR injury. [GRAPHICS]