Liraglutide-induced reduction of myocardial ischemiareperfusion injury in rats via ERK1/2 signaling pathway

Purpose: To investigate the protective effect of liraglutide on myocardial ischemia reperfusion (I/R) injury and its molecular mechanism.
Methods: Ischemia reperfusion model male Sprague-Dawley (SD) rats were randomly divided into negative control group, I/R group (saline), liraglutide group (liraglutide) and PD group (liraglutide + PD98059). The weight of myocardium in ischemic and infarction areas of the heart, myocardial injury biomarker, oxidative stress, as well as expressions of mRNA molecules of apoptosis were determined.
Results: The myocardial mass of ischemic and infarcted areas of the heart (relative to left ventricular mass) of I/R group were significantly higher (p ˂ 0.05) than those of negative control group, but significantly lower in liraglutide group than in I/R group (p > 0.05). However, the parameters were significantly higher in PD group than in liraglutide group (p ˂ 0.05). CK, CK-MB and LDH activities, as well as levels of cTnI and cTnT in I/R group were significantly higher (p ˂ 0.05) than those of negative control group. However, the parameters were significantly lower (p ˂ 0.05) in liraglutide group than in I/R group, but higher in PD group (p ˂ 0.05) than in liraglutide group. Serum SOD, GSH-Px, CAT activities and tBcl-2 mRNA expression were significantly lower in I/R group than those of negative control group (p ˂ 0.001), while those PD group were significantly lower than those of liraglutide group (p ˂ 0.001).
Conclusion: Liraglutide alleviates myocardial ischemia-reperfusion injury and inhibits oxidative stress and apoptosis via ERK1/2 signaling pathway in rats, but further studies are required to ascertain the clinical efficacy and safety of the compound.

Keywords
Ischemia-reperfusion injury; Liraglutide; ERK1/2 signal pathway; Oxidative stress; Apoptosis