Phycocyanin relieves myocardial ischemia-reperfusion injury in rats by inhibiting oxidative stress

Abstract

Purpose: To investigate the effect of phycocyanin on myocardial ischemia-reperfusion injury, and the possible mechanisms involved.
 Methods: Twenty-four Sprague-Dawley (SD) rats were randomly divided into Sham group (only threading without ligation), IRI group (myocardial ischemia-reperfusion injury group) and phycocyanin group (phycocyanin pretreatment + myocardial ischemia-reperfusion injury group). The heart was harvested and cardiomyocytes were isolated. Colorimetry was used to determine the contents of cardiomyocyte serum creatine phospho-MB (CK-MB), lactate dehydrogenase (LDH) and malondialdehyde (MDA), and the activities of total antioxidant capacity (T-AOC), catalase (CAT), glutathione (GSH), total superoxide dismutase (SOD) and other related oxidative stress indicators. Furthermore, apoptosis was evaluated using TUNEL staining. Protein levels of cardiac factor E2 related factor 2 (Nrf2), heme oxygenase-1 (HO-1), human NADPH dehydrogenase 1 (NQO1) and nuclear factor-κB (NF-κB) were evaluated by Western blot and immunohistochemistry.
 Results: Compared with the myocardial IRI group, the contents of CK-MB, LDH, MAD and ROS in the treated group were significantly decreased (p < 0.05), but the activities of SOD, GSH, SOD, CAT, and T-AOC in the myocardial tissues were significantly enhanced (p < 0.05). Moreover, the pathological changes in myocardial tissue were significantly reduced. In addition, the expression levels of Nrf2, HO-1 and NQO-1 were significantly up-regulated after phycocyanin pretreatment, while expression of NF-κB was significantly down-regulated (p < 0.05).
 Conclusion: Phycocyanin improves myocardial anti-oxidative stress via activation of Nrf2 signaling pathway, and also protects rats from myocardial ischemia-reperfusion injury by reducing inflammatory response via inhibition of NF-κB signaling pathway.