Characterization of the intestinal absorption of morroniside from Cornus officinalis Sieb. et Zucc via a Caco-2 cell monolayer model.

Morroniside is a biologically active polyphenol found in Cornus officinalis Sieb. et Zucc (CO) that exhibits a broad spectrum of pharmacological activities, such as protecting nerves, and preventing diabetic liver damage and renal damage. However, little data are available regarding the mechanism of its intestinal absorption. Here, an in vitro human intestinal epithelial cell model of cultured Caco-2 cells was applied to study the absorption and transport of morroniside. The effects of donor concentration, pH and inhibitors were investigated. The bidirectional permeability of morroniside from the apical (AP) to the basolateral (BL) side and in the reverse direction was studied. When administered at three tested concentrations (5, 25 and 100 µM), the apparent permeability coefficient (Papp) values in the AP-to-BL direction ranged from 1.59 × 10-6 to 2.66 × 10-6 cm/s. In the reverse direction, BL-to-AP, the value was ranged from 2.67 × 10-6 to 4.10 × 10-6 cm/s. The data indicated that morroniside transport was pH-dependent. The permeability of morroniside was affected by treatment with various inhibitors, such as multidrug resistance protein inhibitors MK571 and indomethacin, as well as the breast cancer resistance protein inhibitor apigenin. The mechanisms of the intestinal absorption of morroniside may involve multiple transport pathways, such as the passive diffusion and efflux protein-mediated active transport especially involving multidrug resistance protein 2 and breast cancer resistance protein. After the addition of CO, the Papp values in the AP-to-BL direction increased significantly, therefore, it can be assumed that some ingredients in the CO promote morroniside absorption in the small intestine.

[Genotype and phenotype study of two patients with 22q11.2 deletion syndrome].

OBJECTIVE: To carry out genetic analysis for two patients affected with congenital heart disease, developmental delay with or without cleft palate. METHODS: Cytogenetic and molecular genetic methods including karyotyping, fluorescence in situ hybridization (FISH), multiplex ligation-dependent probe amplification (MLPA) and single nucleotide polymorphisms array (SNP-array) were employed to detect potential mutations. For parents of both patients, MLPA was used to analyze whether they were carrier of the deletion. RESULTS: For neither patient, no abnormality was detected upon karyotype analysis. However, FISH analysis has indicated the presence of 22q11.2 deletion. SNP-array analysis has confirmed that both patients have carried a 2.5 Mb deletion in the 22q11.2 region. MLPA analysis suggested none of the parents has carried the same deletion. CONCLUSION: Although the phenotypes of our patients were not identical, they were both diagnosed as 22q11.2 deletion syndrome by multiple methods. The deletions in both cases were de novo in nature. Precise delineation of the genotype can facilitate better understanding of the patients' phenotype.