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    題名: Sperm DNA fragmentation negatively correlates with velocity and fertilization rates but might not affect pregnancy rates
    作者: Huang, CC;Lin, DPC;Tsao, HM;Cheng, TC;Liu, CH;Lee, MS
    貢獻者: 醫學院醫學系;Lee Womens Univ, Div Infertil Clin, Taichung 406, Taiwan;Chung Shan Med Univ, Inst Biochem, Taichung, Taiwan;Chungtai Inst Hlth Sci & Technol, Dept Med Technol, Taichung, Taiwan;Chung Shan Med Univ Hosp, Dept Obstet & Gynecol, Taichung, Taiwan;China Med Univ, Dept Med, Taichung, Taiwan
    日期: 2005
    上傳時間: 2010-09-24 14:51:57 (UTC+8)
    出版者: ELSEVIER SCIENCE INC
    摘要: Background: Paclitaxel, an antineoplastic drug, inhibits cell growth and cell cycle progression and induces apoptosis in human leukemia HL-60 cells. Caspase-3 plays a direct role in proteolytic cleavage of cellular proteins responsible for progression to apoptosis. Methods: We examined the cell morphology and apoptosis in HL-60 cells after exposure to paclitaxel and measured caspase-3 activities with or without z-VAD-fmk (a broad-spectrum caspase inhibitor) pretreatment by flow cytometric analysis and Western blotting. Results: Together, our results were (1) paclitaxel mainly induced G2/M cell cycle arrest in HL-60 cells (p < 0.001); (2) time (p < 0.001)- and dose-dependent (p < 0.001) apoptosis of HL-60 cells was induced by paclitaxel; (3) in HL-60 cells, z-VAD-fmk blocked paclitaxel-induced apoptosis (12 h: p < 0.001; 24 h: p < 0.01; 48 h: p < 0.01; 72 h: p < 0.001) and caspase-3 activation (12 h: p < 0.05; 24 h: p < 0.01; 48 h: p < 0.01; 72 h: p < 0.01). Conclusions: These results suggest that paclitaxel can induce G2/M cell cycle transition and apoptosis via caspase-3 activity in HL-60 cells. (c) 2005 Elsevier B.V. All rights reserved.
    關聯: FERTILITY AND STERILITY 84(1):130-140
    顯示於類別:[醫學系] 期刊論文

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