β-amyloid (Aβ)-mediated neuronal apoptosis contributes to the progression of Alzheimer's disease (AD), although the exact mechanism remains unclear. This study aimed to investigate whether Dalesconol B (TL-2), a potent immunosuppressive agent with an unusual carbon skeleton, could inhibit Aβ-induced apoptosis in vitro and in vivo and to explore the underlying mechanisms. Aβ 1–42 was injected to bilateral hippocampus of mice to make the AD models in vivo. TL-2 was able to cross the blood-brain barrier and attenuate memory deficits in the AD mice. TL-2 also inhibited Aβ 1–42-induced neuronal apoptosis in vitro and in vivo. In addition, TL-2 could activate the AKT/GSK-3β pathway, and inhibition of AKT and activation of GSK-3β partially eliminated the neuroprotective effects of TL-2. Furthermore, TL-2 induced the nuclear translocation of β-catenin and enhanced its transcriptional activity through the AKT/GSK-3β pathway to promote neuronal survival. These results suggest that TL-2 might be a potential drug for AD treatment.

The effects of microalloying elements, Y(0.02at%, 0.04at% and 0.06at%) and Nb(0.2at%, 0.5at% and 0.8at%) on the wettability of intermetallic Fe-40A1 with polycrystalline α-Al2O3 were investigated experimentally by means of sessile drop method. The addition of 0.02at%Y and 0.04at%Y showed no significant effects on the wettability. However, the addition of 0.06at%Y improved the wettability in temperature range from 1673K to 1823K. The addition of different amount of Nb were not beneficial to the FeAl-Al2O3 wettability under conditions investigated. The SEM study of the shear fractured surfaces showed that the additions of Y and Nb coursed Al2O3 particles more adherent to FeAl matrix, compared with the case of pure Fe-40A1. The degree of adherence varied with the amount of Y and Nb. These phenomena are discussed in terms of interfacial reactions and interfacial bonding.