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癌细胞诱导凋亡
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     Research on NDGA's Inducing Apoptosis of Colon Cancer Cell Line HT-29, Mechanis of This Apoptosis and Influence on Its Metastasis
     NDGA对HT-29结肠癌细胞诱导凋亡、凋亡机制及对其转移影响的研究
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     Objective: To study the cell apoptosis of newcastle disease virus (NDV) on the human lines of oral squamous cell carcinoma( OSCC).
     目的检测鸡新城疫病毒(newcastle disease virus,NDV)对人口腔鳞癌细胞诱导凋亡作用。
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     Research on apoptosis of colon cancer cell line HT-29 induced by NDGA
     脂氧合酶抑制剂NDGA对HT-29结肠癌细胞诱导凋亡的研究
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     Research on apoptosis mechanism of HT-29 colon cancer cell induced by NDGA
     脂氧合酶抑制剂NDGA对HT-29结肠癌细胞诱导凋亡机制研究
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     Methods:Using invert microscope,HE stain and acridine orange(AO)/ethidium bromide(EB)fluorescence stain to examine the inhibiting proliferation and inducing apoptosis effct of grub extract on MGC-803 gastric cancer cells.
     方法 :通过倒置显微镜、HE染色、吖啶橙 (AO) /溴化乙锭 (EB)荧光染色方法检测蛴螬提取物对MGC - 80 3胃癌细胞诱导凋亡和抑制作用的方式 ;
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     Inducing effect of resveratrol on anoikis of gastric cancer cells
     白藜芦醇诱导癌细胞脱落凋亡
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     Finally, lead to the articular cartilage
     诱导软骨细胞凋亡
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     The effects of hyperthermia on apoptosis in human colonic carcinoma cell line Lovo
     加热诱导结肠癌细胞Lovo凋亡的研究
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     Peroxisome proliferator-actived receptor-γ ligand troglitazone induces apoptosis in renal cell carcinoma
     曲格列酮诱导癌细胞凋亡
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     Apoptotic Induction of Xinjiang Shikonin on Human Colorectal Cancer CCL229 Cell
     新疆紫草素诱导人大肠癌细胞凋亡
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Objective To investigate induction of apoptosis and its possible mechanism in amiloride treated ovarian carcinoma cell line. Methods Morphological changes of apoptotic cells were investigated by light and fluorescence microsopy. DNA fragmentation was analysed by agarose gel electrophoresis. In addition, the number of hypodiploid cells (apoptotic cells) was quantitatively assessed by flow cytometry and intracellular pH was also analysed. Results Amiloride treated ovarian carcinoma cells showed morphological...

Objective To investigate induction of apoptosis and its possible mechanism in amiloride treated ovarian carcinoma cell line. Methods Morphological changes of apoptotic cells were investigated by light and fluorescence microsopy. DNA fragmentation was analysed by agarose gel electrophoresis. In addition, the number of hypodiploid cells (apoptotic cells) was quantitatively assessed by flow cytometry and intracellular pH was also analysed. Results Amiloride treated ovarian carcinoma cells showed morphological characateristics of apoptosis. A ladder like pattern of DNA fragmentation was demonstrated on agarose gel electrophoresis. Amiloride at 0.01~5 μmol/L could induce apoptosis in 18.7%~61.6% of ovarian carcinoma cells. The apoptosis inducing effect of amiloride was dose and time dependent. In addition, amiloride induced intracellular acidification in a subpopulation of the treated cells. Furthermore, these isolated acidified cells revealed chromatin condensation as well as DNA degradation with characteristics of apoptosis. There was good correlation between apoptotic cells and acidic cells. Conclusion Amiloride triggers apoptosis of ovarian carcinoma cells; intracellular acidification may be involved in the mechanism of apoptosis.

目的观察利尿药氨氯吡咪(amiloride)诱导卵巢癌细胞凋亡及其可能的机理。方法用光镜及荧光显微镜从形态上了解凋亡的发生,用琼脂糖凝胶电泳进一步检测发生凋亡的特征性DNA降解。流式细胞术定量分析用不同剂量氨氯吡咪处理的卵巢癌细胞诱导的凋亡发生率,同时检测被处理细胞细胞内pH。结果氨氯吡咪处理的卵巢癌细胞在形态学上显示出凋亡细胞的特征,琼脂糖凝胶电泳显示特征性DNA阶梯图。流式细胞术检测表明,0.01~5μmol/L氨氯吡咪能诱导18.7%~61.1%卵巢癌细胞发生凋亡,凋亡发生随用药剂量及药物作用时间增加而增多。氨氯吡咪处理的卵巢癌细胞细胞内pH值降低,并出现一群酸化细胞,经分选而分离出的酸化细胞逐渐表现出染色质的浓缩、致密及DNA降解等凋亡特征。这群酸化细胞与凋亡细胞有很好的相关性(r=0.96)。结论氨氯吡咪能诱导卵巢癌细胞凋亡,可能与其降低细胞内pH有关。

Objective To study the effects of arsenic trioxide (As 2O 3) on gastric cancer cells in induction of apoptosis.Methods Apoptosis and cell cycle changes of MKN 45 and MKN 28 induced by As 2O 3 were investigated by TUNEL method and flow cytometry.Results After 12 hours of exposure to the drug, MKN 45 and MKN 28 exhibited morphologic features of apoptosis, including cell shrinkage, nuclear condensation, DNA fragmentation and formation of apototic bodies. A typical subdiploid peak before G 0/G 1 phase...

Objective To study the effects of arsenic trioxide (As 2O 3) on gastric cancer cells in induction of apoptosis.Methods Apoptosis and cell cycle changes of MKN 45 and MKN 28 induced by As 2O 3 were investigated by TUNEL method and flow cytometry.Results After 12 hours of exposure to the drug, MKN 45 and MKN 28 exhibited morphologic features of apoptosis, including cell shrinkage, nuclear condensation, DNA fragmentation and formation of apototic bodies. A typical subdiploid peak before G 0/G 1 phase was observed by flow cytometry. The apoptic index was 7-15% by TUNEL and FACS assay.Conclusions Arsenic trioxide can induce apoptosis of gastric cancer cells and it might have a promising prospect in the treatment of gastric cancer, and worth further studies.

目的 研究三氧二化砷 (氧化砷 )对胃癌细胞的诱导凋亡作用。方法 应用TUNEL染色、流式细胞仪技术研究氧化砷对胃癌细胞MKN 45、MKN 2 8的诱导凋亡作用。结果 氧化砷作用于不同分化程度的胃癌细胞后 ,可看到较为典型的细胞凋亡的形态学变化 :细胞核固缩 ,染色质凝集 ,呈新月型紧贴于核膜周边 ,核碎裂 ,染色质片断化 ,凋亡小体形成等。流式细胞仪DNA直方图上出现典型的亚二倍体的“凋亡峰”。TUNEL染色法显示 ,细胞凋亡指数在 1.4%~ 9.5 %之间。结论 氧化砷对胃癌细胞具有诱导细胞凋亡的作用 ,具有治疗胃癌的潜在价值 ,值得进一步研究。

Purpose; To study the apoptosis induced by paclitaxel and modulation of paclitaxel on telomerase activity in human gastric carcinoma cell line SGC-7901. Methods: Human gastric carcinoma cell line SGC-7901 was treated with paclitaxel (0.001, 0.01, 0.1 and 1 μM) for 1-4 days. MTT assay was used to determine the cell growth inhibition rate, cell morphologic changs were examined under light microscope. Flow cytometry was used to examine bcl-2 gene and paclitaxel-induced apoptosis in gastric carcinoma cell line SGC-7901....

Purpose; To study the apoptosis induced by paclitaxel and modulation of paclitaxel on telomerase activity in human gastric carcinoma cell line SGC-7901. Methods: Human gastric carcinoma cell line SGC-7901 was treated with paclitaxel (0.001, 0.01, 0.1 and 1 μM) for 1-4 days. MTT assay was used to determine the cell growth inhibition rate, cell morphologic changs were examined under light microscope. Flow cytometry was used to examine bcl-2 gene and paclitaxel-induced apoptosis in gastric carcinoma cell line SGC-7901. Also telomerase activity was detected by semi-quantity TRAP assay at the same time. Results; Paclitaxels (0.01 - 1 μM) were cytotoxic to human gastric carcinoma cell in time-dependent and dose-dependent manner. SGC-7901 cell line treated with paclitaxel was induced cell cycle arrest at G2/M phase, leading to apoptosis. At the same time, decreased telomerase activity was detected in paclitaxel-induced apoptotic cell after 24 h, telomerase activity became negative after 72 h. The expression of bcl-2 gene was decreased after paclitaxel treatment. Conclusion: Paclitaxel is effective in growth inhibition on gastric cacinoma cell line. Paclitaxel-induced apoptosis and inhibition of telomerase activity may be one of the anti-cancer mechanisms, bcl-2 is involved in the regulation of telomerase activity during SGC-7901 cell line apoptosis induced by paclitaxel.

目的:研究紫杉醇对人SGC-7901胃癌细胞的诱导凋亡作用及对端粒酶活性调节的关系。方法:0.001~1μM的紫杉醇处理SGC-7901细胞后,用MTT法则定胃癌细胞的生长抑制率,甲苯胺蓝染色后光镜下观察细胞凋亡形态变化,流式细胞仪检测细胞周期、细胞凋亡率及bcl-2水平,半定量TRAP-银染法测定端粒酶活性变化。结果:0.01~1μM的紫杉醇对胃癌细胞均有明显抑制作用。抑制作用首先表现为G2/M期阻滞,继而出现细胞凋亡,且呈时间依赖性及剂量依赖性。对端粒酶活性的同步检测结果显示,紫杉醇在诱导细胞凋亡的同时伴随端粒酶活性下调,且抑制作用逐渐增强,24小时酶活性开始受抑制,72小时变为阴性。在这一过程中,bcl-2表达水平下降。结论:紫杉醇对胃癌细胞具有明显抑制作用,诱导细胞凋亡并抑制端粒酶活性可能是其发挥抗癌作用的机制之一;bcl-2参与了紫杉醇诱导的胃癌细胞凋亡过程中端粒酶活性的调控。

 
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