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3501. [Induction of NAD(P)H: quinone reductase by anticarcinogenic ingredients of tea].
By assaying the activity of NAD(P)H: quinone reductase (QR) in Hep G2 cells exposed to inducing agents, a variety of ingredients in tea, we compared their abilities on inducing QR and preventing cancer. The results showed that tea polyphenols, tea pigments and mixed tea were all able to induce the activity of QR significantly. The single-component ingredients of tea polyphenols and tea pigments, including thearubigens, EGCG and ECG, also enhanced the activity of QR. But EGC, EC, theaflavins, tea polysaccharide and tea caffeine, showed no apparent induction of QR. We found that among those tea ingredients studied, the multi-component ingredients were more effective than the single-component ones. So we thought that the abilities of antioxidation and cancer prevention of tea depended on the combined effects of several kinds of active ingredients, which mainly include tea polyphenols and tea pigments.
3502. [Preheating decrease the sensitivity of K562 cell to chemotherapeutic drugs].
Hyperthermia is a powerful tool for enhancing the effect of many chemical drugs on killing cells, but too many times of hyperthermia could decrease the effect and increase the ability of tumor cell against chemical drugs. Heat stress protein 70(HSP70) mRNA of K562 cell was analyzed by RT-PCR, and the chemosensitivity of K562 cell was tested by MTT method before and after heat-exposure. The results showed that HSP70 mRNA increased greatly after K562 cells exposed to 40 degrees C for 30 min and then it went to the top after 120 min heat-exposure. The sensitivity of K562 cell to adriamycin (ADM) and cyclophosphamide (CTX) in a usual dosage (1/250 of one dosage in clinical use) was in middle degree before exposed to heat, and the sensitivity dramatically went down after K562 cell being heat-stressed. The sensitivity of heat-stressed tumor cells to chemotherapeutic drugs was decreased, which may come from the increased expression of stress proteins in cells.
3503. [The uptake characteristics of 5-fluorouracil in the Caco-2 model system].
The uptake characteristics of 5-fluorouracil in the Caco-2 model system were studied. The uptake of 5-fluorouracil was determined at different pH and concentrations, and in the presence of various inhibitors. The results indicated that the uptake of 5-fluorouracil was the best at pH 6.0. The rate of uptake was saturable with a Km of 24 mmol.L-1, and a Vmax of 20.9 nmol.min-1.mg-1 protein. The uptake was inhibited by noncompetitive inhibitors such as NaCN, ouabain, and dipyridamole. The uptake was also inhibited competitively by analogous compounds such as uracil, thymine, and uridine (but not by hypoxanthine). In conclusion, the evidence suggests that 5-fluorouracil was transported by uracil carrier in Caco-2 cells.
3504. [Recent development in quinolone compounds antitumor quinolones].3505. [A new method for study of the effect of drugs on cancer cells--31PNMR with perfused cell system].
31P NMR was performed for the studies on the metabolic changes of endogenous phosphorus-containing molecules in KB and HCT-8 cells exposed to taxol at a concentration of 10(-6) mol.L-1. Using the perfusion method, the cells can be detected for a longer time by NMR, so as to give continuous spectra of the two cell-lines during the perfusion with and without the drug. The spectra showed that the levels of ATP peaks for both cells enhanced during the perfusion with the drug, but the change of the level is more prominent in KB cells than in HCT-8 cells. This shows that KB cells are more sensitive to taxol than HCT-8 cells. This is in coincident with the result in the cytotoxicity studies. However, the experiment using vincristine at the same concentrations demonstrated that the level of the ATP peak was not changed significantly.
3506. [Synthesis and biological activity of 2,3-benzopyrone analogs].
Several 2, 3-benzopyrone analogs were synthesized for evaluating their K(+)-channel and anticancer activities. The Friedel-Crafts reaction was taken place with some replacement phenyl acetic acid or its methyl ester and vanillin as reactants in the condition of Ac2O/ZnCl2. All products were confirmed by means of MS and 1H, 13CNMR spectra. Compounds 2 and 3 showed obvious activities on the K(+)-channel and anticancer screening, while the activity of compound 5 was weak. Compound 4 was not yet tested. The primary result indicate that the potential activity of such compounds deserves further study.
3507. [Anti-invasion activity of several plant-originated anticancer drugs with different mechanism of action].
The antitumor and anti-invasion activities of taxol, harringtonine, homoharringtonine and camptothecin on highly metastatic melanoma B16-BL6 and human fibrosarcoma HT-1080 cells were reported in this paper. Results demonstrated that taxol, harringtonine, homoharringtonine and camptothecin exhibited significant inhibition of cell growth of B16-BL6 and HT-1080 cells. Taxol, harringtonine and homoharringtonine were also found to be effective for the inhibition of cell invasion and migration of B16-BL6 cells, but camptothecin showed basically no effect at the indicated concentration.
3508. [Enhanced cytotoxicity of VM-26 in human malignant glioma cells by calcium channel blocker nicardipine in vitro].
Using the monolay tumor cell culture system and the method or MTT colorimetric analysis, the cytotoxicity of the anticancer drug VM-26 and Nicardipine(NCDP) in human malignant glioma cell line U251 was studied. The results showed that the cytotoxicity of VM-26 in U251 was enhanced by NCDP at a low dose which did not show direct cytotoxicity. The authors considered that VM-26 combined with NCDP can heighten the intracellular anticancer drug concentration, reverse the drug resistance and heterogeneity in human malignant glioma cells. The mechanism of the enhanced effect was also discussed. These findings will provide an alternative chemotherapeutic clue to treat the postoperative malignant gliomas.
3509. [Antimetastatic effects of arginine-aspartate on salivary adenoid cystic carcinoma in vitro].
To test the effects of arginine-aspartate (RD) on metastasis of salivary cystic carcinoma (SACC).
3510. [Assessment of six drug sensitivities in established cell lines of SO-Rb50 and SO-Rb70].
With retinoblastoma (Rb) cell lines cultured in vitro to screen chemotherapeutic drugs that are effective on Rb.
3511. [Effect of inhibition of telomerase activity on cisplatin-induced apoptosis in K562 cells].
To explore the effect of human telomerase reverse transcriptase (hTERT) gene antisense oligodeoxynucleotide (ASODN) on telomerase activity and cisplatin-induced apoptosis in K562 cells.
3512. [Aminopeptidase inhibitor Bestatin induces HL-60 cell apoptosis through activating caspase 3].
To study the variation and significance of caspase 3 activity in the process of amino-peptidase inhibitor--bestatin (BS) inducing human leukemic cell apoptosis.
3513. [In vitro cotransfer human multidrug resistance gene (mdr-1) and dihydrofolate reductase gene (DHFR) into human CD(34)(+) progenitor cells to broaden the spectrum of drug resistance].
To explore the feasibility of cotransferring human mdr-1 gene and DHFR gene into human CD(34)(+) progenitor cells to broaden the spectrum of drug resistance and improve the tolerance of myelosuppression following combination chemotherapy.
3514. [Study on the relationship between apoptosis and reactive oxygen species of cancer cell lines induced by anticarcinogens].
作者: L Cai.;S Gao.;Y Yang.;D Zheng.;W Wang.;G Zhang.;Q Fuyong.
来源: Zhonghua Xue Ye Xue Za Zhi. 2001年22卷5期249-51页
To investigate the relationship between apoptosis (AP) and fluorescent intensity of reactive oxygen species (ROS) in cancer cell lines induced by anticancer agents, and the mechanisms of drug sensitivity and resistance.
3515. [Inhibition of proliferation and induction of apoptosis by simvastatin in K562 leukemic cell line].
To investigate the anti-apoptotic mechanism and explore approach to inhibiting proliferation and inducing apoptosis of chronic myclogenous leukemia (CML) cells.
3516. [Protection of hematopoietic stem cells by MIP-1alpha and PF4 against the cytotoxicity of chemotherapeutic agents].
To study the protective effects of macrophage inflammatory protein-1alpha (MIP-1alpha) and platelet factor 4 (PF4), alone and in combination, on hematopoietic stem/progenitor cells against the cytotoxicity of chemotherapeutic drugs.
3517. [Altered subcellular distribution of daunorubicin in the non-P-glycoprotein-mediated multidrug-resistant cell line HL-60/ADR].
作者: Y Gong.;Y Wang.;F Chen.;J Han.;N Shao.;Z Fang.;R Ouyang.
来源: Zhonghua Xue Ye Xue Za Zhi. 2000年21卷6期309-11, 2页
To investigate DNR subcellular distribution in the non-P-glycoprotein-mediated multidrug-resistant cell line HL-60/ADR and its relation to multidrug resistance.
3518. [Taxol-induced apoptosis in Jurkat T cell lymphoma cell line and its molecular mechanisms].
作者: X Zhou.;L Xu.;K He.;T Zhang.;W Zhu.;X Li.;A Jin.
来源: Zhonghua Xue Ye Xue Za Zhi. 2000年21卷6期298-300页
To observe whether antimicrotubular drug taxol can induce apoptosis in Jurkat T cell lymphoma cell line and the role of bcl-2 gene family in this process.
3519. [Mobilization of autologous peripheral blood stem cells by chemotherapy and recombinant granulocyte colony-stimulating factor (G-CSF) and granulocyte-macrophage colony-stimulating factor (GM-CSF)].
作者: X Cui.;Y Shao.;B Ren.;Z Tong.;X Ren.;L Li.;Z Zhang.;N Zhang.;R Dai.;X Hao.
来源: Zhonghua Xue Ye Xue Za Zhi. 2000年21卷5期247-9页
To observe the efficacy of chemotherapy and recombinant granulocyte colony-stimulating factor (G-CSF, Glycosylated) and granulocyte-macrophage colony-stimulating factor (GM-CSF) in autologous peripheral blood stem cells (APBSC) mobilization.
3520. [Mechanism of tissue factor expression on NB4 cells down-regulated by all-trans retinoic acid and arsenic trioxide].
作者: W Guo.;H Wang.;W Zhao.;B Qu.;L Pan.;J Zhu.;H Chu.;X Wang.
来源: Zhonghua Xue Ye Xue Za Zhi. 2000年21卷5期240-3页
To investigate molecular mechanism of tissue factor (TF) expression on acute promyelocytic leukemia cell line NB4 cells down-regulated by all-trans retinoic acid (ATRA) and arsenic trioxide (As(2)O(3)).
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