ABSTRACT
Objective: To investigate the effects of baicalin on the cell cycle and apoptosis of human colon cancer in vitro and in vivo, and to further clarify its possible molecular mechanism. Methods: After treatment with different concentrations (0, 50, 100, 200, 400 and 800 μg/mL) of baicalin for 48 h, the morphology and viability of human normal colorectal mucosa FHC cells and human colon cancer HCT116 cells were detected by invert microscopy and MTT method, respectively. The changes of apoptosis rate and cell cycle distribution of HCT116 cells after baicalin treatment were detected by flow cytometry. The expression levels of apoptosis-related proteins [poly ADP-ribose polymerase-1 (Parp-1), caspase 3, X-linked inhibitor of apoptosis protein (XIAP), nuclear factor-κB (NF-κB), p53, Bcl-2 and Bax] and cell cycle-related proteins (cyclin D1 and cyclin B1) in HCT116 cells treated with baicalin were measured by Western blotting. After the orthotopic xenograft tumor model of colon cancer HCT116 cells in nude mice were constructed and treated with baicalin by gavage, the body weight of mice and the tumor size were checked, and the baicalin-induced apoptosis in xenograft tumors was also assayed using TUNEL methods. Results: As compared with baicalin-untreated control group, 50-800 μg/mL baicalin significantly suppressed the viability of colon cancer HCT116 cells (all P 0.05). Conclusion: Baicalin can inhibit the growth of colon cancer HCT116 cells in vivo and in vitro through inducing apoptosis and cell cycle arrest at G1 phase.
ABSTRACT
Objective To explore the distribution of inflam m atory cells and positive expression of P-se-lectin glycoprotein ligand-1 (PSG L-1) in infant brainstem tissue from hand-foot-m outh disease related fatal brainstem encephalitis. Methods Tw enty brainstem sam ples from infants suffered from brainstem en-cephalitis w ere collected as the experim ental group. Ten brainstem sam ples from infants died of non-brain diseases and injuries w ere collected as the control group. The distribution of inflam m atory cells and the expression of PSG L-1 in the tw o groups w ere exam ined by im m unohistochem ical m ethod. The characteristics of the positive cells w ere observed. Results In brainstem tissue of the experim ental group, there w ere sleeve infiltrations of inflam m atory cells around the vessels and in the glial nodule. Microglia was the m ost and following was neutrophils around the vessels and in the glial nodule. There was a significant statistical difference am ong m icroglias, neutrophils and lym phocytes (P<0.05). There was no sleeve infiltration in the control group. PSG L-1 protein was expressed w idely in inflam m atory cells in the experim ental group, especially in the inflam m atory cells around the vessels and in the glial nodule. B ut PSG L-1 positive staining could be observed significantly less in the control group com paring with the experim ental group (P<0.05). Conclusion Microglia is the m ain type of inflam m atory cells involved in the progress of the fatal disease. Moreover, PSG L-1 could participate in the pathogenesis of hand-foot-m outh disease related fatal brainstem encephalitis.