ABSTRACT
There is a broad and urgent need for the clinical application of anticancer nanomedicine in tumor therapy, but the complex biological barrier in solid tumors has always been the main obstacle to infiltrating nanomedicine into the tumor. The traditional design of nanomedicine based on enhanced permeability and retention (EPR) effect still has some limitations in tumor permeability, it is urgent to find other design theories. Therefore, this review summarizes two novel strategies, active transcytosis and immune cell-mediated tumor penetration, for promoting tumor penetration of anticancer nanomedicine.
ABSTRACT
To investigate the chemical constituents of Anisodus tanguticus, silica gel column chromatography, Sephadex LH-20 column chromatography, preparative thin layer chromatography, and semi-preparative HPLC were used to separate and purify the chemical constituents from the extract of A. tanguticus. The planar structure of the isolated compound was identified by HRMS, IR, and 2D NMR experiments. The absolute configuration of the isolated compound was determined by a combination of NOESY, coupling constant, circular dichroism (CD), and transition metal chelate reagent dimolybdenum tetraacetate [Mo2(OAc)4]-induced circular dichroism (ICD) data analysis. A new compound of the anisotane-type sesquiterpene (1) was isolated, which was determined to be (1R,2S,3R,4R,6R,7R,9R)-anisotane-11(13)-ene-3,4,9-triol and named anisotanol F. This is the second report of anisotane-type sesquiterpene, which has previously been reported as a novel sesquiterpenoid skeleton by our research group. Furthermore, the cytotoxicity against HUVECs and inhibitory effect on NO release in LPS-induced RAW264.7 cells of compound 1 were investigated. However, the results showed that it was inactive. Compound 1 is a new compound isolated from A. tanguticus. It belongs to the unusual anisotane-type sesquiterpene. This result enriches the chemical composition of A. tanguticus.
ABSTRACT
Objective: To determine the role of p38 mitogen-activated protein kinase (MAP) kinase signal transduction pathways in epigallocatechin-3-gallate (EGCG)-induced apoptosis in human gastric cancer MGC803 cells. Methods: The viability of MGC803 cells was measured by MTT assay. Apoptosis of MGC803 cells was observed by AO/EB fluorescence microscopy and detected by flow cytometry with PI staining. Expression of p38MAPK and phosphorylated p38 (pp38) MAPK were determined by Western blot analysis. Results: EGCG induced apoptosis of MGC803 cells and apparently increased the activity of pp38MAPK in MGC803 cells. However, after interference with pp38MAPK inhibitor, the inhibitory effect of EGCG on MGC803 cells was significantly weakened. The apoptotic rate of the cells and the activity of pp38MAPK also decreased dramatically. Conclusions: EGCG can induce apoptosis of MGC803 cells. The effects could be markedly suppressed by pp38MAPK inhibitor, SB203580. EGCG induces apoptosis of MGC803 cells partly by activating p38 MAPK.