Structure and antioxidant activity of polysaccharide POJ-U1a extracted by ultrasound from Ophiopogon japonicus.

An ultrasonic technique was employed to extract polysaccharides from Ophiopogon japonicus. The ultrasonic extracted polysaccharides (POJ-U) were purified, and POJ-U1a (a homogeneous fraction) was obtained. The structural characteristics of POJ-U1a were investigated by infrared spectra, gas chromatography, high performance liquid chromatography, periodate oxidation, Smith degradation, methylation analysis, gas chromatography-mass spectrometry and nuclear magnetic resonance spectroscopy. The results indicated that the relative molecular weight of POJ-U1a was 4.02×10(3)Da. POJ-U1a was an α-configuration polysaccharide with a highly branched structure, and consisted of pyranoside and funanside. The backbone of POJ-U1a consisted of 1,6-α-d-glucopyranose and 1,3,6-α-d-glucofuranose in the molar ratio of 7:3, while the branched chains were mainly composed of 1,3-α-d-glucopyranose and 1-α-d-glucopyranose in the molar ratio of 1:3. The branched structure of POJ-U1a was proved intuitively by AFM. Significant antioxidant activity of POJ-U1a has been proved as shown by its DPPH radical scavenging, hydrogen radical scavenging and superoxide anion scavenging activities, which indicated that POJ-U1a showed strong antioxidant activity.

Static magnetic fields enhanced the potency of cisplatin on k562 cells.

PURPOSE: This study investigates whether 8.8 mT static magnetic fields (SMFs) can enhance the killing potency of cisplatin (DDP) on human leukemic cells (K562). METHODS: The cell proliferation, cell cycle distribution, DNA damage, and the change in cell surface ultrastructure after K562 cells were exposed to 8.8 mT SMFs with or without DDP were analyzed. RESULTS: The results show that SMFs enhanced the killing effect of DDP on K562 cells, reducing the efficient killing concentration of DDP on K562 cells from 20 to 10 microg/mL. Atomic force microscope observation showed that the cell surface ultrastructure was altered. The results of fluorescence-activated cell sorting analysis indicated that K562 cells treated with SMF plus DDP were arrested at the S phase. The SMF exposure induced DNA to become thicker than controls, and breakage of DNA occurred in the DDP group; however, DNA breakage was increased in the SMF + DDP group. CONCLUSIONS: The results show that SMFs enhanced the anticancer effect of DDP on K562 cells. The mechanism correlated with the DNA damage model. This study also shows the potentiality of SMFs as an adjunctive treatment method for chemotherapy.