In conclusion, we have shown that open abdominal surgery, in the absence of general anesthesia, induced an age-dependent neuroinflammation and changes in CD33 levels in the hippocampus of mice. The aged mice are more vulnerable to the peripheral surgical wounding-induced neuroinflammation and increases in CD33 levels. Ibuprofen, an antiinflammatory drug, ameliorated the peripheral surgical woundinginduced cognitive impairment in aged mice. Taken together, these findings carry insightful implications for the surgical care of elderly patients and suggest that the aging brain could be more susceptible to the development of neuroinflammation following peripheral surgical wounding. Pending further studies, it may be useful to consider anti-inflammatory to reduce the risk of POCD in elderly patients. Myocardial infarction is defined as a clinical event caused by coronary thrombosis, and subsequent myocardial ischemia in which there is evidence of myocardial injury or necrosis. Two major causes of coronary thrombosis are plaque rupture and endothelial erosion. Recent studies have shown that inflammation plays a key role in the pathogenesis of both plaque rupture and endothelial erosion. Activated immune cells produce various inflammatory molecules and proteolytic enzymes that can weaken the fibrous cap and activate cells in the core, transforming the stable plaque into a vulnerable, unstable structure that can rupture, induce a thrombus, and elicit an acute myocardial infarction. Because inflammation plays a key role in the pathogenesis of acute MI, a 
relevant biomarker of immune activation may provide novel prognostic information in these patients. CD93 is a 68 kDa transmembrane glycoprotein and is expressed in monocytes, leukocytes, and endothelial cells. CD93 is over-expressed upon inflammatory stimulation, and the soluble form is known to be increased in various inflammatory conditions. It has been shown that sCD93 induces the differentiation of monocytes into macrophage-like cells that have increased phagocytic activities and enhanced cell adhesion, and it has been implicated in inflammation and inflammatory Coptisine-chloride diseases such as rheumatoid arthritis. A recent study demonstrated that CD93 is correlated with the risk of coronary artery disease. In a genetic replication study, van der Net et al. reported that patients homozygous for the T-allele of the CD93 genetic polymorphism had a 26% increased risk of CAD compared with patients with at least one C-allele. Significant associations between plasma sCD93 levels, premature MI, and the incidence of CAD were reported in two independent cohorts. Also, it has been demonstrated that the minor allele of an single nucleotide polymorphism in the 39 untranslated region of the CD93 gene was associated with increases in both plasma sCD93 concentration and CD93 mRNA expression levels in peripheral blood mononuclear cells. These data suggest that genetic polymorphisms of CD93 and circulating sCD93 levels are associated with CAD in cross-sectional studies. However, the relationship between sCD93 and the prognosis of acute MI has never been investigated. Therefore, in the present study, we examined if the circulating level of sCD93 is increased in acute MI patients. In addition, to explore the Isoacteoside possible underlying mechanism leading to increased sCD93.