ABSTRACT
Objective To study the mechanism of tumor necrosis factor-related apoptosis-inducing ligand(TRAIL)-induced apoptosis of glioma U87 cells.Methods Human glioma U87 cells were treated with human recombinant soluble TRAIL(rsTRAIL),and the cell apoptosis was detecmd with flow cytometry with AnnexinV-FITC/PI double staining.Flow cytometry with DiOC6 staining was used to assess the changes in mitochondrial transmembrane potential(△ψm).The relative activity of caspase-3,-8 and-9 Was measmed by colorimetric assay,and the concentration of cytoplasmic cytochrome C(cyt C) determined using enzyme-linked immunosorbem assay.The effects ofcaspase-8 inhibitor(Z-IETD-fmk)on rsTRAIL-induced apoptosis,△ψm,caspase-3,-8 and-9 activities and cyt C concentration were observed. Results RsTRAIL tinle-dependently induced apoptosis and progressive collapse of △ψm in glioma U87 cells,resulting also in caspase-3,-8 and-9activation and elevated cytC concentration.Caspase-8 inhibitor partially antagonized these biological effects induced by rsTRAIL in U87 cells.Conclusion TRAIL initiates a cascade of mitochondrial events by activating caspase-8 and induces apoptosis of glioma U87 cells.
ABSTRACT
To study the gene polymorphism of HLA-A, B, DRB1 alleles in patients with chronic myelogenous leukemia and to explore the correlation of HLA with chronic myelogenous leukemia, the polymerase chain reaction-reverse sequence specific oligonucleotide (PCR-RSSO) was used to analyze the polymorphism of HLA-A, B, DRB1 alleles of 293 CML Patients and 406 randomized and synchronous blood donors (healthy and unrelated with patients) from Guangdong Han population. The results indicate that the gene frequency of HLA-A*24 in CML group was 15.53% lower than that of control group (22.09%, RR = 0.63, p = 0.005); the gene frequency of HLA-B*13 in CML group was 10.41% higher than that of control group (6.74%, RR = 1.68, p = 0.016). The gene frequency of HLA- DRB1*14 in CML group was 7.51% lower than that of control group (11.89%, RR = 0.58, p = 0.008). The differences were all statistically significant. It is concluded that the gene frequency of HLA-A*24, HLA- DRB1*14 in CML patients is significantly lower than normal people in Guangdong. The gene frequency of HLA-B*13 in CML patients is significantly higher than normal people in Guangdong. Further study is needed to make sure whether HLA-A*24 and HLA- DRB1*14 are protective gene markers for CML acquisition on Guangdong Chinese Han population and whether HLA-B*13 is a gene marker for CML susceptibility on this population.