Pholiols E-K, lanostane-type triterpenes from Pholiota populnea with anti-inflammatory properties.

Investigation of the chloroform and ethyl acetate extracts of the edible mushroom Pholiota populnea led to the isolation of eight triterpenes, the undescribed natural products pholiols E-K and the known (+)-clavaric acid. HRESIMS and 1D and 2D NMR spectroscopy were employed to determine the structures of the undescribed compounds. The NOESY spectra were used to assign the relative configurations of triterpenes.

Triterpenes from as Cytotoxic Agents and Chemosensitizers to Overcome Multidrug Resistance of Cancer Cells.

The detailed mycochemical analysis of the -hexane extract of led to the isolation of four new lanostane diesters, named pholiols A-D (-), together with an acyclic triterpene, (3,6,10,14,18,22)-2,3,22,23-tetrahydroxy-2,6,10,15,19,23-hexamethyl-6,10,14,18-tetracosatetraene (), ergosterol (), and 3β-hydroxyergosta-7,22-diene (). The isolation was carried out by multistep flash chromatography, and the structures were elucidated using extensive spectroscopic analyses, including 1D and 2D NMR and MS measurements. The isolated metabolites (-) were investigated for cytotoxic activity against Colo205 and Colo320 colon adenocarcinoma and nontumoral MRC-5 cell lines.

Fingolimod, a sphingosine-1 phosphate receptor modulator, increases BDNF levels and improves symptoms of a mouse model of Rett syndrome.

The functional relevance of brain-derived neurotrophic factor (BDNF) is beginning to be well appreciated not only in mice, but also in humans. Because reduced levels typically correlate with impaired neuronal function, increasing BDNF levels with well-tolerated drugs diffusing into the central nervous system may help in ameliorating functional deficits. With this objective in mind, we used the sphingosine-1 phosphate receptor agonist fingolimod, a drug that crosses the blood-brain barrier.

Disease modeling using embryonic stem cells: MeCP2 regulates nuclear size and RNA synthesis in neurons.

Mutations in the gene encoding the methyl-CpG-binding protein MECP2 are the major cause of Rett syndrome, an autism spectrum disorder mainly affecting young females. MeCP2 is an abundant chromatin-associated protein, but how and when its absence begins to alter brain function is still far from clear. Using a stem cell-based system allowing the synchronous differentiation of neuronal progenitors, we found that in the absence of MeCP2, the size of neuronal nuclei fails to increase at normal rates during differentiation.