Inhibition of TRAF3 expression alleviates cardiac ischemia reperfusion (IR) injury: A mechanism involving in apoptosis, inflammation and oxidative stress

摘要: Abstract Ischemia reperfusion (IR) injury is known as a major issue in cardiac transplantation and various pathogenesis are involved myocardial IR injury. Here, we show that tumor necrosis factor receptor-associated 3 (TRAF3) was increased hearts of mice with cardiomyocytes incubated lipopolysaccharide (LPS) H2O2. Reducing TRAF3 expression in vivo markedly reduced the infacrted area, attenuated histological changes, improved dysfunction subjected to Functional study further indicated knockdown inhibited apoptosis murine LPS H2O2-cotreated cardiomyocytes, evidenced by decreased cleaved Caspase-3 poly (ADP-ribose) polymerases (PARP). In addition, inflammatory response oxidative stress observed operation were significantly alleviated through inhibiting nuclear factor-κB (NF-κB) xanthine oxidase (XO) signaling pathways, similar results detected in vitro. Moreover, loss also restrained phosphorylated c-Jun N-terminal protein kinase (JNK) activation following Importantly, blocking JNK activation, knockdown, greatly apoptosis, inflammation reactive oxygen species (ROS) production cardiomyocytes. contrast, knockdown-reduced rescued promoting activity summary, our repressing could be served essential therapeutic target for protection against restraining JNK-meditated ROS.