Hydrogen-bonded six-component assembly for capsule formation based on tetra(4-pyridyl)cavitand and isophthalic acid linker and its application to photoresponsive capsule.

Two molecules of tetra(4-pyridyl)cavitand 1 and four molecules of isophthalic acid linker 2a with a triethylene glycol monomethyl ether (TEG) group self-assembled into a six-component capsule 12·2a4 through eight pyNHO2C hydrogen bonds, which encapsulates one molecule of guest G such as bis(4-acetoxyphenyl)acetylene and hexakis(4-iodophenyl)benzene to form G@(12·2a4). Guest-encapsulation ability and selectivity of 12·2a4 were revealed. trans-5-(p-Substituted-phenylazo)isophthalic acid with two dichotomous branching TEG groups trans-2b serves as a photoresponsive linker to form 12·(trans-2b)4, which moderately reduced guest-encapsulation ability upon photoisomerization (at the photostationary state, 10% guest release upon subunit-trans-2b/subunit-cis-2b = 18 : 82).

1'-Acetoxychavicol acetate ameliorates age-related spatial memory deterioration by increasing serum ketone body production as a complementary energy source for neuronal cells.

1'-Acetoxychavicol acetate (ACA) is naturally obtained from the rhizomes and seeds of Alpinia galangal. Here, we examined the effect of ACA on learning and memory in senescence-accelerated mice prone 8 (SAMP8). In mice that were fed a control diet containing 0.02% ACA for 25 weeks, the learning ability in the Morris water maze test was significantly enhanced in comparison with mice that were fed the control diet alone. In the Y-maze test, SAMP8 mice showed decreased spontaneous alterations in comparison with senescence-accelerated resistant/1 (SAMR1) mice, a homologous control, which was improved by ACA pretreatment. Serum metabolite profiles were obtained by GC-MS analysis, and each metabolic profile was plotted on a 3D score plot. Based upon the diagram, it can be seen that the distribution areas for the three groups were completely separate. Furthermore, the contents of ß-hydroxybutyric acid and palmitic acid in the serum of SAMP8-ACA mice were higher than those of SAMP8-control mice and SAMR1-control mice. We also found that SAMR1 mice did not show histological abnormalities, whereas histological damage in the CA1 region of the hippocampus in SAMP8-control mice was observed. However, SAMP8-ACA mice were observed in a similar manner as SAMR1 mice. These findings confirm that ACA increases the serum concentrations of ß-hydroxybutyric acid and palmitic acid levels and thus these fuels might contribute to the maintenance of the cognitive performance of SAMP8 mice.