Effect of Parecoxib Sodium on Myocardial Ischemia-Reperfusion Injury Rats.

BACKGROUND 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.

[Anesthetic effects of repeated dosing with propofol and vitamin C in mice].

OBJECTIVE: To explore the anesthetic effects of repeated administration of propofol combined with vitamin C in mice. METHODS: Forty mice were subjected to daily intraperitoneal injections of 80 mg/kg propofol (P80 group), 70 mg/kg propofol and 50 mg/kg vitamin C (P70+Vc50 group), 55 mg/kg propofol and 100 mg/kg vitamin C (P55+Vc100 group), or 50 mg/kg propofol and 200 mg/kg vitamin C (P50+Vc200 group) for 6 consecutive days, and the anesthesia induction time and anesthesia duration were recorded. RESULTS: Compared with the P80 group, the mice in P55 + Vc100 group and P50 + Vc200 group showed significantly shorter anesthesia duration on the first 3 days (P<0.05). In all the groups, anesthesia duration was significantly shortened in the following days compared with that on day 1 (P<0.01); anesthesia duration was shorter on day 3 than on day 2 in P50 + Vc200 group (P<0.01), and was shorter on days 4, 5, and 6 than on day 2 in all the groups (P<0.01). In all the groups, the rate of loss of righting reflex (LORR) decreased gradually with time in a similar pattern. CONCLUSION: Vitamin C can reduce the dose of propofol without obviously affecting the anesthetic effect to reduce the incidence of drug tolerance and potential dose-related side effects of propofol.