期刊文献+

软骨多糖对L1210细胞增殖抑制作用的研究

Study on the growth inhibitory effects of cartilage polysaccharide on L1210 cells
下载PDF
导出
摘要 建立DBA/2小鼠LI210腹水瘤模型,将小鼠分为5组进行实验,通过腹腔注射软骨多糖治疗,每天称重并记录小鼠的生存时间,计算生命延长率。于0h、24 h、48 h、72 h抽取治疗组小鼠的腹水瘤细胞进行吉姆萨(Giemsa)染色观察细胞形态学变化;应用TUNEL和免疫荧光方法检测细胞凋亡和凋亡相关蛋白表达的变化,以进一步探讨软骨多糖的抑瘤机制。结果表明:软骨多糖可以显著提高DBA/2小鼠的生命延长率;细胞形态学观察可见细胞出现细胞浆浓缩、核固缩及凋亡小体等现象;软骨多糖作用后凋亡细胞逐渐增多,72 h凋亡率与0 h相比差异显著(P<0.01);Bax蛋白的表达水平于给药后升高,抗凋亡基因Bcl-2表达下降。软骨多糖可能通过影响肿瘤细胞线粒体凋亡途径相关的Bax、Bcl-2蛋白的表达来诱导L1210细胞凋亡,并显著抑制肿瘤细胞的生长。 To investigate the growth inhibitory effect of cartilage polysaccharide on L1210 leukemia mice,and discuss its anti-tumor mechanism.DBA/2 mouse model was established using mouse L 1210 cells.Mice were divided into 5 groups,and were treated by i.P.injection of cartilage polysaccharide.Body weight was measured every day and survival time was recorded.The increase of lifespan was calculated.Giemsa staining were performed using ascites got-from the mouse in treated group at 0 h,24 h,48 h and 72 h to observe the changes of morphology.The apoptotic cells were detected by TUNEL assay and the expression of Bax and Bcl-2 proteins were studied by immunofluorescent technology to explore the anti-tumor mechanism of cartilage polysaccharide.The survival rate of L1210-bearing mice increased significantly by treatment of cartilage polysaccharide.Cell shrinkage,nuclear condensation and apoptotic body could be detected by cell morphological observation.The apoptotic rate significantly increased on 72 h vs.0 h(P〈0.01).The expression of Bax protein was up-regulated after treatment of cartilage polysaccharide as well as the expression of Bcl-2 expression was low-regulated. Apoptosis of L1210 cells can be induced by cartilage polysaccharide through the effect on the expression of Bax an d Bcl-2 proteins,and the great inhibition on tumor cell growth.
作者 杨宁 刘安军
出处 《中国科技论文在线》 CAS 2009年第9期684-690,共7页
基金 国家自然科学基金(20776113) 高等学校博士学科点专项科研基金(20050057002)
关键词 软骨多糖 L1210细胞 凋亡 BCL-2 BAX cartilage polysaccharide L1210 cells apoptosis Bc1-2 Bax
  • 相关文献

参考文献5

二级参考文献76

共引文献159

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部