Was still significantly higher compared with the shamoperated group (Figure 3A). Then Western Blot was

Was still significantly higher compared with the shamoperated group (Figure 3A). Then Western Blot was applied to determine whether upregulation of COX2 mRNA resulted in increased synthesis of COX2 protein. As a result, the COX2 protein expression in the rat SC144 web hippocampus was similar to the COX2 mRNA expression. The COX2 protein expression peaked at 7 d after I/R and decreased at 15 d (Figure 3B).Expression of COX2 protein (by immunohistochemistry) in rat hippocampus at different time points after reperfusionsignificant increase of number of cells that express COX2, but PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/27532042 an increase of expression in the same population of cells (Figure 4A). The COX2 in the CA1 significantly increased at 30 min (P < 0.05) and peaked at 7 d (P < 0.01), and thereafter decreased at 15 d, but was still significantly higher compared with the sham-operated group (P < 0.01) (Figure 4B).The expression of COX2 was in the cytoplasm. In the sham group, there was only a faint expression of COX2 in CA1, but COX2 expression increased rapidly in hippocampus CA1 following global ischemia. There was noDiscussion Oxidative stress has emerged as a key deleterious factor in brain I/R [32]. Ischemic brain injury leads to the overproduction of free radicals [33], which damage cell membranes as well as DNA and proteins by initiating lipid peroxidation [34]. Brain in particular is highly susceptible to free radical-mediated insult, owing to its high content of unsaturated fatty acids and low levels of protective antioxidants. SOD which is a specific scavengerFigure 3 Time course change of COX2 mRNA (A) and protein (B) expression in I/R rat hippocampus. COX2 mRNA and protein remarkably increased at 30 min, and reached the peak at 7 d after I/R injury when compared with that of sham operation group. (Compared with the sham group, *P < 0.05, **P < 0.01).Yu et al. Behavioral and Brain Functions 2014, 10:42 http://www.behavioralandbrainfunctions.com/content/10/1/Page 7 ofFigure 4 Time course change of COX2 protein expression in hippocampus of I/R rat. (A) Time course change of COX2 protein expression in I/R rat hippocampus. (B) Group data showing the time course change of COX2 protein expression. Compared with that of sham operation group, COX2 protein remarkably increased at 30 min after I/R, and reached the peak at 7 d after I/R. (Compared with the sham group, *P < 0.05, **P < 0.01).of superoxide anion is involved in the regulation of antioxidant defenses by catalyzing the dismutation of superoxide anion into H2O2 and O2 [35]. MDA is one end product and the biomarker of lipid peroxidation [36]. The SOD activities and MDA contents reflect the balance between oxidative and antioxidative levels in the brain. Our experiments showed a sustained elevation of MDA content and a steady decrease of SOD activity following I/R injury. Our findings are consistent with previous findings, such as that the increased level of lipid peroxidation persists for several days following a brief forebrain ischemia in the gerbil hippocampus [37]. These results together show that ischemic brain injury will lead to the overproduction of free radicals if not cleared timely, and will disturb the balance between oxidative and antioxidative levels in the brain. Accumulated evidence suggests that the enhanced COX2 participates in the development of neuronal deathand in brain ischemia and neurodegenerative diseases [38,39]. Zhao et al. [40] found that the number of COX2 immunostained cells increased at 12 h, peaked a.