ABSTRACT
<p><b>OBJECTIVE</b>To investigate quinalizarin-induced apoptosis in gastric cancer cells in vitro and explore the molecular mechanisms.</p><p><b>METHODS</b>MTT assay was used to determine the cytotoxic effects of quinalizarin on human gastric cancer AGS, MKN-28 and MKN-45 cells. Annexin V-FITC/PI staining and flow cytometry were used to assess quinalizarin-induced apoptosis in AGS cells and its effect on intracellular ROS levels; the expression levels of apoptotic proteins in the cells were determined with Western blotting.</p><p><b>RESULTS</b>Quinalizarin dose-dependently reduced the cell viabilities of the 3 gastric cancer cells (P<0.05). The ICvalues of quinalizarin in AGS, MKN-28 and MKN-45 cells were 7.07 µmol/L, 22.55 µmol/L and 14.18 µmol/L, respectively. Quinalizarin time-dependently induced apoptosis of AGS cells and potentiated the generation of intracellular reactive oxygen species (ROS) levels. Pretreatment with NAC, a scavenger of ROS, inhibited quinalizarin-induced apoptosis (P<0.001). Western blotting results showed that quinalizarin also up-regulated the expression levels of the apoptotic proteins including p-p38, p-JNK, Bad, cleaved caspase-3, and cleaved PARP-1 (P<0.05), and down-regulated the expression of the anti-apoptotic proteins p-Akt, p-ERK, and Bcl-2 (P<0.05).</p><p><b>CONCLUSION</b>Quinalizarin inhibits the proliferation and induces apoptosis in gastric cancer cells in vitro through regulating intracellular ROS levels via the MAPK and Akt signaling pathways.</p>
ABSTRACT
<p><b>OBJECTIVE</b>To characterize the differential and proliferative activities of FLK-1(+) cells derived from mouse fetal liver.</p><p><b>METHOD</b>The FLK-1(+) fraction were enriched from the fetal liver using immunomagnetic method and their differential and proliferative activities were examined in culture medium and in vivo via transplantation of FLK-1(+) cells into the inferior pole of the spleen of nine-week-old male C57 BL/6 mice after two-thirds hepatectomy.</p><p><b>RESULTS</b>In response to growth factors, FLK-1(+) cells expressed typical lineage-specific markers for vascular endothelial cells, smooth muscle cells. Intrahepatic implantation of FLK-1(+) cells resulted in the formation of blood vessels in the fibrous capsule of partially hepatectomized liver.</p><p><b>CONCLUSION</b>These results indicate that FLK-1(+) cells derived from mouse fetal liver could differentiate into endothelial cells and smooth muscle cells and they may serve as potential stem cells for clinical cell-based therapy.</p>
