Recently, the diverse effects of several constituents of KRG, including ginsenoside, on endothelial cells have been extensively studied. Hien et al demonstrated the anti-inflammatory

and antiatherosclerotic activities of ginsenoside Rg3 in human endothelial cells, with a decrease of cell adhesion molecules and proinflammatory cytokines [36]. Moreover, the cytoprotective effect of ginsenoside Rb1 in endothelial cell damage mediated by oxidized low-density lipoprotein has been reported [37]. Several constituents of red ginseng have been reported to regulate proliferation and migration and to protect oxidative stress-mediated damage in human endothelial cells [38] and [39]. There is evidence demonstrating

the presence of major ginsenosides including Rb1 and Rg1 in KRG water extract [40]. Thus, these components could also contribute to the diverse Nivolumab retinue of protective actions of KRG. A previous study showed that the induction of HO-1 expression may exert protective effects in KRG-treated human endothelial cells [19]. The inhibitory effect of KRG on inflammatory responses has also been reported. However, there have been no reports revealing the mechanism underlying KRG-inhibited COX-2 expression in acrolein, α,β-unsaturated aldehydes in CS, stimulated HUVECs. We find more have established that the major signaling pathway of COX-2 (i.e., p38 MAPK–CREB) and intracellular ROS generation

are involved in this inhibition of COX-2 expression in acrolein-stimulated HUVECs by KRG. As mentioned above, KRG also exerts preventive effects on apoptosis induced by acrolein. Therefore, the inhibition of COX-2 expression following KRG water extract treatment may be associated with its strong protective effect in acrolein-stimulated HUVECs. In conclusion, we propose that the KRG water extract may exert a cytoprotective effect through the inhibition of COX-2 induction and that this reduction of COX-2 in acrolein-stimulated HUVECs is mediated by the p38 MAPK–CREB pathway. This study suggests a possible therapeutic mechanism of KRG in vascular Thalidomide diseases. All authors have no conflicts of interest to declare. This work was supported by the 2012 grant from the Korean Society of Ginseng. “
“Influenza viruses belong to the Orthomyxoviridae with genomic negative-sense ribonucleic acid. They are classified as A, B, and C by antigenic differences in their nucleocapsid (NP) and matrix (M) proteins [1]. Influenza A viruses are circulating in aquatic birds and have been responsible for human pandemics. Sixteen subtypes of hemagglutinin (HA) and nine subtypes of neuraminidase (NA) of influenza A viruses have thus far been described in aquatic birds [2] and [3]. Influenza pandemics in humans by influenza A viruses occur three to four times per century.