Rapidly and accurately quantitative analysis of whole-cell sugars in some strains of actinomycetes by GC-MS was performed in this paper. After the polysaccharides were hydrolyzed, deoxidized and esterified , the alditol acetate derivates was analyzed by GC-MS. The derivates of rhamnose, ribose, arabinose , xylose, madurose, mannose, glucose, galactose were separated commendably under this condition. The ratio of the peak area was calculated to get the relative percentage of the various sugars.

Four impurities were isolated from raw material of clindamycin phosphate (CP), and their structures have been determined. LC-MS was used to determine the molecular weights of the impurities in the raw material of CP. Reversed-phase preparative HPLC was used to prepare them, and their chemical structures were identified by HR-MS and NMR. The four unknown impurities were determined as clindamycin-B-phosphate (1), clindamycin-2,4-diphosphate (2), 3',6'-dehydro clindamycin phosphate (3), epi-clindamycin phosphate (4). Impurity 1 has been included in BP and EP, while 2, 3 and 4 have not. The impurities 2, 3, 4 are first separated from raw material of CP.

Objective:To investigate the inhibitory effect of esomeprazole on proliferation and chemosensitizing effect of breast cancer cells.Methods:Human MBA-MD-231, MCF-7 breast cancer cell line and human Huh7 liver cancer cell line were cultured by conventional methods; cells were treated with different concentrations of esomeprazole, and CCK8 kit was used to detect the proliferation of different tumor cells after stimulation. Cells were treated with different concentrations of esomeprazole, and the effects of esomeprazole on cell cycle of different cells were analyzed by flow cytometry. Cells were treated with different concentrations of paclitaxel and epirubicin combined with esomeprazole, and CCK8 kit was used to detect the proliferation of different tumor cells after stimulation. Measurement data were expressed as mean ± standard deviation ( ± s), and analysis of variance was used for comparison among multiple groups. Results:CCK8 results showed that esomeprazole could inhibit the proliferation of MBA-MD-231 cells, MCF-7 cells and Huh7 cells in a dose-dependent manner. Flow cytometry results showed that cells in G 0/G 1 phase were significantly increased by esomeprazole treatment. Esomeprazole can enhance the inhibitory effect of paclitaxel and epirubicin on the proliferation of MBA-MD-231 cells and MCF-7 cells, and improve the chemosensitivity. Conclusion:Esomeprazole blocks breast cancer cell MBA-MD-231, MCF-7 and liver cancer cell Huh7 in G 0/G 1 phase, thereby inhibiting cell proliferation. Esomeprazole can enhance the inhibitory effect of chemotherapeutic drugs on the proliferation of MBA-MD-231 and MCF-7 cells.