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Publications (8)12.3 Total impact

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    ABSTRACT: Luteolin (Lu) exhibits a wide spectrum of anti-tumor activities, the present study was to observe whether Lu can sensitize breast cancer cells to doxorubicin (Dox) and to explain the basis underlying this phenomenon. In vitro, Lu at dose less than 100 microM had only slight effect on cells growth and cytotoxicity of Dox in 4T1 and MCF-7 cells under normoxia, but it could reverse tumor resistance to Dox and promote death of tumor cells under hypoxia. In vivo, Lu alone had also no effect on tumor growth delay, however, it could offer superior efficacy and lesser toxicity of Dox in 4T1 and MCF-7 bearing mice. Further study showed that Lu was able to suppress glycolytic flux but did not affect glucose uptake, the P-glycoprotein, anti-oxidative enzymes under hypoxia in vitro, and had not also effect on the intratumor Dox level in vivo. In addition, the activity of SOD and CAT was increased in serum and was decreased in tumor by Lu in vivo. These results suggest that luteolin as a glycolytic inhibitor might be a new adjuvant agent for chemotherapy.
    Biochemical and Biophysical Research Communications 09/2008; 372(3):497-502. · 2.28 Impact Factor
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    ABSTRACT: To evaluate the therapy action of Sal-Ammoniac extract on Lewis lung cancer and its toxicity to immunity. The proliferation and cell cycle of Lewis lung cancer cells were determined by MTT assay and flow cytometry respectively. The antitumor effect of Sal-Ammoniac extract was observed by tumor injected subcutaneously in mice and its toxicity to immunity was examined by clearance rate of charcoal particles and delayed type hypersensitivity. Sal-Ammoniac extract could inhibit the proliferation of Lewis lung cancer cells with S cell cycle arrest in a dose-dependent manner in vitro. Sal-Ammoniac extract solution injected in tumor for eight days had 46.7% inhibition on Lewis lung cancer, if taken orally had only 15.7% inhibition on Lewis lung cancer in mice. Sal-Ammoniac extract solution injected subcutaneously or taken orally had no effect on the clearance rate of charcoal particles and delayed type hypersensitivity in mice. The antitumor action of Sal-Ammoniac extract has relation to its recipe and has no influence on immunity.
    Zhong yao cai = Zhongyaocai = Journal of Chinese medicinal materials 03/2008; 31(2):245-8.
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    ABSTRACT: To observe inducing differention effect on cells of serum from mice treated with Yang He decoction (SMY). The viability of B16 cells was tested by lactate dehydrogenase (LDH) release assay and sulforhordamine B (SRB) assay. The differentiation of 3T3-L1 preadipocyte, HL-60, K562 and B16 cells were assessed by microscopy and Oil red O staining, NBT reduction and phagocytosis, haemoglobin (Hb) content and melanin content, respectively. SMY could obviously inhibit growth of B16 cells without cytotoxicity, and promote Oil red O staining in 3T3-L1 preadipocyte, enhance the NBT reduction ability and the phagocytosis of horse radish peroxidase in HL-60 cells, increase Hb content in K562 cells, and decrease melanin content in B16 cells. SMY is able to induce functional differentiation and maturation of 3T3-L1 preadipocyte and tumor cells, which implies the major mechanism of Yang He decoction in antitumor.
    Zhong yao cai = Zhongyaocai = Journal of Chinese medicinal materials 02/2008; 31(1):82-5.
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    ABSTRACT: A series of six novel 5-fluorouracil derivatives 1-6 were synthesized and their structures confirmed by (1)H- and (13)C-NMR, MS and elemental analysis. The preliminary in vitro antitumor activities against B16, K562 and CHO cells and the in vivo inhibitions of liver cancer H(22) demonstrated that some of these compounds effectively inhibit the growth of tumor cells, but the in vivo trials in mice revealed that the compounds also exhibited serious liver and lung tissue toxicity. The hydrolysis experiments indicated that this type of compound did not readily liberate 5-fluorouracil, as expected.
    Molecules 02/2007; 12(11):2450-7. · 2.43 Impact Factor
  • Molecules. 01/2007; 12(11):2450-2457.
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    ABSTRACT: Bcl-2 is best known for its anti-apoptotic function in a wide variety of cell types. The objective of this study was to investigate the effects of bcl-2 on the types of cell demise in the HeLa/bcl-2 cells induced by H2O2. The HeLa cell expressed stably bcl-2 was established and defined as the HeLa/bcl-2 cell strain, while the cell transfected with the empty expression vector was defined as the HeLa/vector cell strain. MTT assay revealed that the HeLa/bcl-2 cells showed a shorter life span. BrdU incorporation assay indicated that the bcl-2 exerted anti-demise effect on the HeLa/bcl-2 cells at the low concentration of H2O2. However, at the high concentration of H2O2, the death of the HeLa/bcl-2 cells was more than that of the HeLa/vector cells. The flow cytometry demonstrated that H2O2 mainly induced apoptosis in the HeLa/vector cells and elicited necrosis in the HeLa/bcl-2 cells. The addition of celecoxib to the cells treated by H2O2 could increase apoptosis in the HeLa/vector cells and convert necrosis into apoptosis in the HeLa/bcl-2 cells. The higher levels of cellular free radical and GSH were found in the HeLa/bcl-2 cells, but not in the HeLa/vector cells. With 200 microM H2O2 challenge for 48 h, the level of the cellular free radical was increased in the both strains, while the level of the GSH was decreased in the both strains. Celecoxib could reverse the difference between the both strains led by H2O2. Western blotting showed that the expression of COX-2 was always higher in the HeLa/bcl-2 cells than in the HeLa/vector cells under the both of treated and untreated with H2O2, while the level of COX-1 was relative stable in the both strains. These results suggested that the crosstalk between the bcl-2 and the COX-2 pathways could exist, the bcl-2 might up-regulate COX-2 to modify sensitivity to the types of demise in the HeLa/bcl-2 cell.
    Cancer Letters 03/2006; 232(2):179-88. · 4.26 Impact Factor
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    Yi-ming Yang, Gang-jun Du, Hai-hong Lin
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    ABSTRACT: To study the therapeutic effect of thalidomide (Tha) on murine hepatocellular carcinoma. In murine transplanted hepatoma model, thalidomide was administered intragastrically alone (200 mg/kg daily for 10 days) or in combination with doxorubicin. The antitumor activity of Tha was observed in solid and ascitic tumor models. Tha induced significant growth inhibition of solid hepatoma without obvious toxicity on peripheral blood cells and lymphocyte proliferation. Although Tha alone had no effect on the survival of mice with ascitic tumor, it showed a synergistic antitumor activity in combination with doxorubicin (Dox) in both solid and ascitic tumor models. Moreover, Tha reduced Dox-induced cytopenia and immunosuppression. Histological analysis of Tha-treated tumors revealed remarkably enhanced tumor necrosis and lymphocyte infiltration on the edge of tumor tissues. Tha has definite therapeutic effect on murine hepatoma, and the combination with Dox shows an enhanced therapeutic potential.
    Di 1 jun yi da xue xue bao = Academic journal of the first medical college of PLA 09/2005; 25(8):925-8.
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    ABSTRACT: Thalidomide is an antiangiogenic drug and is clinically useful in a number of cancers. However, the molecular mechanism by which thalidomide exerts its antitumor effects is poorly understood. This study was designed to clarify the relationship between antiangiogenesis and antitumor effects of thalidomide and to explore the molecular mechanism for its antitumor activity. We evaluated the effects of thalidomide on the growth of human tumor cells expressing (MCF-7 and HL-60) or not expressing (HeLa and K562) COX-2 in vitro. We also studied the effects of thalidomide on COX-1, COX-2 or bcl-2 expression, TNFalpha, VEGF, GSH and cytochrome c in these cells. Thalidomide could inhibit tumor growth in a concentration-dependent manner in MCF-7 and HL-60; its IC50s for them were 18.36+/-2.34 and 22.14+/-2.15 microM, respectively, while this effect was not observed in HeLa and K562. Thalidomide reduced COX-2 expression accompanied by a decrease of bcl-2 protein, TNFalpha, VEGF, GSH and an increased cytochrome c, but had no effect on that of COX-1, in MCF-7 and HL-60. Moreover, cells not expressing COX-2 were insensitive to the growth-inhibitory and effects on cytokines of thalidomide. In our mouse xenograft model of OVCAR-3 and HCT-8, we found that thalidomide could decrease intratumoral microvessel density in both tumors; it exerted antitumor effects only on OVCAR-3 expressing COX-2 but did not on HCT-8 not expressing COX-2. Effect of thalidomide on COX-1 and COX-2 in vivo was consistent with that of in vitro. These results demonstrated that thalidomide might inhibit growth of tumors through COX-2 degradation independent of antiangiogenesis.
    Vascular Pharmacology 09/2005; 43(2):112-9. · 3.21 Impact Factor