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ABSTRACT: The objective of this study was to investigate the protection by naringenin against doxorubicin-induced oxidative damage in normal blood cells. Inhibiting effects of naringenin, doxorubicin and naringenin combined with doxorubicind on K562 cells and polymorphonuclear leukocytes were detected with MTT method, the level of reactive oxygen species (ROS) and lipid peroxidation (MDA), the activity of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were examined with spectrophotometric method in the K562 cells and polymorphonuclear leukocytes. The results indicated that the proliferation of K562 cells was not inhibited by the cytotoxicity of doxorubicin in combination of naringenin with doxorubicin. As compared with the doxorubicin, the addition of naringenin after doxorubicin for 1 hour, the levels of reactive oxygen species (ROS) and lipid peroxidation (MDA) obviously decreased, the activity of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) obviously increased in the polymorphonuclear leukocytes, but these were not changed obviously in K562 cells. It is concluded naringenin can protect against doxorubicin-induced oxidative damage in normal blood cells. The mechanism of naringenin may be elevating activities of antioxidant enzyme and degrading oxidative production level in normal blood cells, and meanswhile decreasing level of oxidative products.
Zhongguo shi yan xue ye xue za zhi / Zhongguo bing li sheng li xue hui = Journal of experimental hematology / Chinese Association of Pathophysiology 09/2008; 16(4):790-3.
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ABSTRACT: To study FANCA protein expression in Fanconi anemia patient's (FA) cells and explore its function.
FANCA protein expression was analyzed in 3 lymphoblast cell lines derived from 3 cases of type A FA (FA-A) patients using Western blot. Nucleus and cytoplasm localization of FANCA protein was analyzed in one case of FA-A which contained a truncated FANCA (exon 5 deletion). The FANCA mutant was constructed from the same patient and its interaction with FANCG was evaluated by mammalian two-hybrid (M2H) assay.
FANCA protein was not detected in the 3 FA-A patients by rabbit anti-human MoAb, but a truncated FANCA protein was detected in 1 of them by mouse anti-human MoAb. The truncated FANCA could not transport from cytoplasm into nucleus. The disease-associated FANCA mutant was defective in binding to FANCG in M2H system.
FANCA proteins are defective in the 3 FA-A patients. Disfunction of disease-associated FANCA mutant proved to be the pathogenic mutations in FANCA gene. Exon 5 of FANCA gene was involved in the interaction between FANCA and FANCG.
Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi 12/2007; 28(11):741-4.
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ABSTRACT: To investigate the anti-chronic myeloid leukemia (CML) effect of cytotoxicity T lymphocytes (CTL) activated by dendritic cells (DC) pulsed with freeze thaw K562 lysates antigen.
DC were achieved by healthy donors peripheral blood monocytes which were induced by granulocyte-macrophage colony stimulating factor (GM-CSF) and IL-4. On the sixth day, these cells were collected. One part of them was used to prove that they were DC from morphology and phenotypes. The other part was pulsed with K562 lysates and the lysate-loaded DC were compared with immature DC from phenotypes. The expression of IL-12 and IFNgamma in supernatant, the mixed lymphocytes reaction and the specific cytotoxicity against leukemia cells were tested.
Freeze thaw K562 lysate up-regulated the expression of various differentiation antigens of DC, such as CD(1a) (27.40 +/- 5.00)% vs (15.40 +/- 2.34)%, CD(80) (61.35 +/- 5.35)% vs (42.00 +/- 2.77)%, CD(83) (93.30 +/- 3.48)% vs (25.15 +/- 4.02)%, CD(86) (85.25 +/- 4.39)% vs (37.25 +/- 3.20)%, CD(40) (89.80 +/- 7.18)% vs (35.95 +/- 4.06)% and HLA-DR (49.50 +/- 5.45)% vs (17.15 +/- 3.61)%. Simultaneously, the expression of IL-12 rose after DC were loaded with tumor lysates after 24 hours (P < 0.05). The T cells from healthy donors and CML patients, proliferated by antigen loaded DC, could induce IFNgamma increase (P < 0.01). The proliferation of T cells had distinct relation with the time of antigen loaded with DC. These T cells had specific cytotoxicity against K562 and HLA partial matching CML cells.
DC pulsed with K562 lysates can stimulate T cells, and can keep high immunocompetence with specific cytotoxicity against K562.
Zhonghua nei ke za zhi [Chinese journal of internal medicine] 12/2006; 45(12):1013-6.
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ABSTRACT: To screen the FANCA gene mutation and explore the FANCA protein function in Fanconi anemia (FA) patients.
FANCA protein expression and its interaction with FANCF were analyzed using Western blot and immunoprecipitation in 3 cases of FA-A. Genomic DNA was used for MLPA analysis followed by sequencing.
FANCA protein was undetectable and FANCA and FANCF protein interaction was impaired in these 3 cases of FA-A. Each case of FA-A contained biallelic pathogenic mutations in FANCA gene.
No functional FANCA protein was found in these 3 cases of FA-A, and intragenic deletion, frame shift and splice site mutation were the major pathogenic mutations found in FANCA gene.
Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi 11/2005; 26(10):616-8.
