Directed C-H Activation and Tandem Cross-Coupling Reactions Using Palladium Nanocatalysts with Controlled Oxidation.

Controlled oxidation of palladium nanoparticles provided high-valent PdIV oxo-clusters which efficiently promote directed C-H halogenation reactions. In addition, palladium nanoparticles can undergo changes in oxidation states to provide both high-valent PdIV and low-valent Pd0 species within one system, and thus a tandem reaction of C-H halogenation and cross-coupling (C-N, C-C, and C-S bond formation) was successfully established.

Rh(0)/Rh(iii) core-shell nanoparticles as heterogeneous catalysts for cyclic carbonate synthesis.

Rh(0)/Rh(iii) core-shell nanoparticles were prepared by surface oxidation of Rh nanoparticles with N-bromosuccinimide. They were employed as heterogeneous catalysts for cyclic carbonate synthesis from propylene oxide and CO2, and exhibited high activity and excellent recyclability due to Lewis acidic Rh(iii) species on the shells.

Kobophenol A enhances proliferation of human osteoblast-like cells with activation of the p38 pathway.

Bone cell proliferation, bone formation, and bone resorption are the main factors involved in the homeostasis of the bone mass. Osteoblast death is a problem experienced by postmenopause women. Herbal medicines have attracted considerable attention for use as a drug or a drug substitute in the treatment of bone-related diseases, such as osteoporosis. This study investigated the effects of kobophenol A on the proliferation in human osteoblast cells. Kobophenol A stimulated the proliferation of osteoblast cells by the increases in DNA synthesis and the enhancement of cell cycle progression. Kobophenol A stimulation induced the expression of the cyclin B1 and cyclin-dependent kinase 1 (CDK1). Treatment of osteoblast cells with p38 MAPK inhibitor SB203580 significantly inhibited kobophenol A-enhanced proliferation. In addition, kobophenol A induced phosphorylation of p38 MAPK. Treatment of osteoblast cells with kobophenol A resulted in improvement of ROS scavenging activity. Moreover, kobophenol A treatment up-regulated the Bcl-2 level, but down-regulated the level of Bax expression. We also demonstrate that kobophenol A increased alkaline phosphatase (ALP) activity after 2 days. Taken together, the results of this study reveal that kobophenol A has proliferative effects and enhances ALP activity in osteoblast cells and these findings provide insights into the development of a therapeutic approach of kobophenol A in the prevention of osteoporosis and other bone disorders.

Diosgenin inhibits macrophage-derived inflammatory mediators through downregulation of CK2, JNK, NF-kappaB and AP-1 activation.

Diosgenin is a precursor of steroid hormones, which can be found in several plant species. Diosgenin has been shown to have a variety of biological activities including anti-inflammatory activity, but through a mechanism that is unclear. Especially, the effect of this agent on macrophage function has not been characterized in detail. In the present study, we examined the effects of diosgenin on the production of inflammatory mediators in lipopolysaccharide (LPS)/interferon gamma (IFN-gamma)-activated murine macrophage. Macrophages pre-exposed to diosgenin (0.1-10 microM) were stimulated with LPS/IFN-gamma. Pretreatment with diosgenin resulted in the inhibition of NO production and inducible nitric oxide synthase (iNOS) protein and mRNA expression in a concentration-dependent manner. In addition, diosgenin inhibits production of reactive oxygen species (ROS), interleukin-1 (IL-1), and IL-6, but not that of tumor necrosis factor-alpha (TNF-alpha). Inhibition of these inflammatory mediators appears to be at the transcriptional level, since diosgenin decreased LPS/IFN-gamma-induced NF-kappaB and AP-1 activity. Diosgenin blocked CK2 activation and phosphorylation of c-Jun NH(2)-terminal kinase (JNK), but not that of p38 mitogen-activated protein kinase (MAPK) and extracellular signal-regulated kinase 1/2 (ERK 1/2). These results indicate that the inhibition of these signaling molecules expression was correlated with the reduced production of inflammatory mediators in macrophages. Taken together the present data suggest that diosgenin reduces the production of inflammatory meditators by inhibiting LPS/IFN-gamma-triggered CK2, JNK, NF-kappaB and AP-1 activation, thereby implicating a mechanism by which diosgenin may exert its immunosuppressive effects.