Myricetin and M10, a myricetin-3-O-ß-d-lactose sodium salt, modify composition of gut microbiota in mice with ulcerative colitis.

Our previous studies found that M10, a myricetin-3-O-ß-d-lactose sodium salt, possessed higher effects of ameliorating ulcerative colitis (UC) than Myricetin in mice. Here, we aim to investigate whether the inhibition of UC is the consequence of the effects of M10 that leads to the changed microbiota. Mice model of UC was induced by dextran sulfate sodium (DSS) treatment. M10 and Myricetin were orally administrated for 12 weeks. We performed 16S rDNA sequencing assay to analyze the composition of gut microbiota isolated from ileocecum. Both M10 and Myricetin normalized the composition of Firmicutes and Actinobacteria as healthy mice had. At genus level, the effects of M10 and Myricetin on colitis were associated to the increase of probiotics, such as Akkermansia, and the inhibition of pathogenic microorganisms, such as Ruminococcus and Parabacteroides. M10 had stronger activity than Myricetin in the improvement of biosynthesis and degradation activities, resulting to increasing metabolism of sulfur, pyruvate, steroid biosynthesis and unsaturated fatty acid biosynthesis in gut. Furthermore, M10 normalized the proportion of Firmicutes and Actinobacteria in gut microbiota. It suggests that the improvements in UC are the consequence of the effect of M10 that leads to the changed intestinal microbiota. Conclusion: M10 contributed the pharmacological effects on UC by modification of the intestinal microbiota.

LHRHa aided liposomes targeting to human ovarian tumor cells: preparation and cellular uptake.

In this study, a synthetic nonapeptide similar to luteinizing hormone-releasing hormone (LHRHa), the ligand of an extracellular membrane receptor specific to ovarian tumor cells, was selected as targeting moiety and electrically adsorbed to the negatively charged liposomes composed of phospholipid and monocholesterolsuccinate. Docetaxel, as the first line chemotherapy for ovarian tumor, was chosen to be encapsulated into the liposomes. And a high encapsulate efficiency (93%) and drug loading efficiency (20%) of liposomes were achieved via central composite design. In order to investigate the targeting efficiency of the drug delivery system, in vitro cell uptake was determined and the results showed an increasing uptake of LHRHa aided liposomes compared to normal ones.

Study on in vivo distribution of liver-targeting nanoparticles encapsulating thymidine kinase gene (TK gene) in mice.

Nanoparticles formulated from polylactic-co-glycolic acid (PLGA) polymer loading a new recombinant plasmid pEGFP-TKAFB (TK-PLGA-NPs) were prepared by a double-emulsion evaporation technique. Both in vitro and in vivo release behaviors of TK-PLGA-NPs (with particle diameter ranged from 50 to 100 nm) were investigated, using ethidium bromide (EB) staining and gamma scintigraphy, respectively. The results indicated that the in vitro release rate of DNA (pEGFP-TKAFB plasmid) in TK-PLGA-NPs showed good fit into the Higuichi Equation and dependence in the molecular weight of PLGA polymer. 0.5 h after injection of nanoparticles containing (32)P labeled pEGFP-TKAFB plasmid ((32)P-TK-PLGA-NP) via caudal vein of the mice, the ratio of radioactivity intensity in the liver to total intensity was above 70%, which showed a 1.4-fold increase over that by injection of (32)P labeled pEGFP-TKAFB plasmid ((32)pEGFP-TKAFB plasmid, (32)P-TK). Similarly, 2 h after hypodermic injection of (32)P-TK-PLGA-NPs in mice, the ratio of radioactivity in the liver against total radioactivity was more than 70%, which was 1.6-fold compared with naked (32)P-TK. All these data showed that the TK-PLGA-NPs has the potential for liver-targeting and delayed drug release.