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作 者:刘琦[1] 刘春敏[1] 姜少军[2] 吴波[2] 孟奎[2] 刘小转[3] 施正良[4] 石群立[2]
机构地区:[1]南京军区南京总医院妇产科,南京210002 [2]南京军区南京总医院病理科,南京210002 [3]南京军区南京总医院生化科,南京210002 [4]南京军区军事医学研究所实验动物中心
出 处:《解放军医学杂志》2005年第3期237-240,共4页Medical Journal of Chinese People's Liberation Army
摘 要:目的 探讨全反式维甲酸干预后卵巢癌细胞株(体外)及裸鼠卵巢上皮性癌动物模型(体内)肿瘤细胞内糖原的变化及 意义。方法 以不同浓度及作用时间的全反式维甲酸对COC2细胞株进行体外干预后,测定细胞质糖原、乳酸脱氢酶含量,并行光 镜、电镜观察;以每只2mg/(kg·d)×4周剂量的全反式维甲酸对CAOV3细胞株荷瘤裸鼠经胃管针给药干预,收集肿瘤标本进行光 镜、电镜、组织化学及免疫组织化学检查。结果 COC2经5μmol/L及10μmol/L全反式维甲酸作用后细胞内糖原含量增加、乳酸脱 氢酶含量下降且均与时间呈正比,在30μmol/L全反式维甲酸作用后细胞则以凋亡为主;CAOV3荷瘤裸鼠经全反式维甲酸干预后,裸 鼠肿瘤细胞同样出现细胞内糖原增加的改变。结论 全反式维甲酸直接用于COC2细胞或经消化道给药间接作用于CAOV3荷瘤 裸鼠肿瘤后,均出现细胞内糖原含量增加、乳酸脱氢酶下降的改变,减缓了肿瘤细胞内的能量代谢,从而起到抑制肿瘤生长的作用。Objective To investigate the effect of all-trans retinoic acid on the change in intracellular glycogen in ovarian epithelioma cell line in vitro and ovarian epithelial carcinoma in nude mice in vivo. Methods COC2 cells were treated with all-trans retinoic acid in 1, 5, 10 and 30μmol/L drug concentrations for different length of time, and then intracellular glycogen and LDH were determined by biochemistry assay. Morphologic changes were observed with light and electron microscopy. CAOV3 tumor-bearing nude mice were treated with intragastric injection of the same drug in a dose of 2mg/(kg·d) for four weeks. The tumor samples were harvested thereafter for pathological study with histochemical and immunohistochemical staining, and also with electron microscopy. Results Intracellular glycogen was significantly increased, while LDH level was lowered after the cell line was treated with 5~10μmol/L of all-trans retinoic acid, and apoptosis of cancer cell occurred after using 30μmol/L of the drug. These changes were also observed in CAOV3 cells of tumor-bearing nude mice. Conclusion Our results suggest that treatment with all-trans retinoic acid resultin an increase in intracellular glycogen and decrease in LDH level both in COC2 cells in vitro and in CAOV3 tumor-bearing nude mice in vivo, and the suppression of tumor cell proliferation may be attributed to retarded intracellular metabolism.
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