Fangyong Wu, Wei Wang, Yingying Duan, Jia Guo, Guanhua Li, Tao Ma
Department of Anesthesiology, Eastern Medical District of Chinese People’s Liberation Army (PLA) General Hospital, Beijing, China (mainland)
Med Sci Monit 2021; 27:e928205
Available online: 2020-11-02
We aimed to explore the effect of parecoxib sodium on myocardial ischemia-reperfusion (I/R) injury rats and its mechanism.
MATERIAL AND METHODS: The coronary artery of Sprague-Dawley rats was occluded for 6 h of myocardial ischemia, followed by reperfusion for 30 min (I/R group). Before ischemia, parecoxib sodium (10 mg/kg) was intraperitoneally injected twice a day for 3 consecutive days, followed by reperfusion for 6 h (I/R+Pare group). The cardiac function and changes in the infarction area were evaluated via echocardiography in each group. The differences in the expressions of apoptosis-related proteins were determined via immunohistochemistry and western blotting. Then, the percentage of reactive oxygen species (ROS)⁺ cells and the content of lipid peroxide were detected, based on which the degree of oxidative stress was evaluated. Next, the expressions of nuclear factor-kappaB (NF-kappaB) and nuclear factor E2-related factor 2 (Nrf-2) signaling pathways and downstream target genes were determined using real-time quantitative polymerase chain reaction (PCR).
RESULTS: After treatment with parecoxib sodium, the cardiac function of I/R injury rats was restored, and the infarction area and apoptosis level were reduced (P<0.05). Parecoxib sodium reduced the levels of ROS and lipid peroxidation in myocardial I/R injury rats, thereby weakening oxidative stress. It also regulated the redox imbalance caused by I/R injury through regulating NF-kappaB and Nrf-2 (P<0.01). In addition, after treatment with parecoxib sodium, NF-kappaB was significantly downregulated, while Nrf-2 was upregulated, and the content of proinflammatory cytokines was obviously reduced (P<0.01).
CONCLUSIONS: Parecoxib sodium exerts a protective effect against myocardial I/R injury through regulating antioxidant and inflammatory mechanisms.
Keywords: NF-E2-Related Factor 2, Receptor Activator of Nuclear Factor-kappa B, Reperfusion Injury