期刊文献+

氯化甲基汞抗裸鼠皮下U251胶质瘤细胞的体内实验研究 被引量:1

The morphology study in apoptosis effect of methyl-mercuric chloride on brain neuroglioma
下载PDF
导出
摘要 目的在建立裸鼠皮下U251胶质瘤模型基础上,通过体内实验及相关形态学研究,分析氯化甲基汞(MMC)的抗脑胶质瘤作用。方法制备裸鼠皮下U251胶质瘤模型,随机分为对照组和实验组,实验组裸鼠注射U251脑胶质瘤细胞1w后,每天灌胃给予10mg/kg体重MMC,连续5d,对照组给予相同体积的生理盐水。全部裸鼠于肿瘤接种后14d处死。结果大体病理显示实验组肿瘤体积明显小于对照组,病理组织学观察发现实验组U251胶质瘤细胞生长密度较对照组低,并可见细胞体积变小、核固缩等凋亡的形态学改变。透射电镜显示实验组肿瘤细胞发生核固缩、染色质周边化、核断裂、胞浆空泡变性等改变,实验组瘤体汞含量明显高于对照组。结论MMC对裸鼠U251胶质瘤细胞增殖具有明显的抑制作用,其机制可能是通过诱导胶质瘤细胞凋亡实现的,相关分子机制有待进一步深入研究。 Objective To study the morphology change in apoptosis effect of methyl-mercuric chloride (MMC) on brain neuroglioma.Methods Experimental group were lavaged with MMC for 5 d and 10 mg/kg BW per day after the conduction of the athymic rat model of neuroglioma,control group was given with sodium chloride at the same dose.Results Oncopathology study showed that the average tumor volume of experimental group was smaller than those in control group obviously,the experimental group showed a lower density and a smaller volume than those in control group from HE stain.The phenomenon of karyopycnosis,liquefaction and anachromasis also could be seen in some cells.The neuroglioma cells were represented pyknosis,chromoplasm margination,nuclear fragmentation and vacuolar degeneration by perspective electron microscope.Conclusions MMC is capable of inhibiting the proliferation of rat C6 neuroglioma cells in vivo.The possible mechanism is that MMC is capable of deducing apoptosis in neuroglioma cells.The molecule mechanism of inhibitory effect of MMC on brain neuroglioma are requested for research to advance.
出处 《中国老年学杂志》 CAS CSCD 北大核心 2010年第5期609-611,共3页 Chinese Journal of Gerontology
基金 国家自然科学基金资助项目(39770655)
关键词 氯化甲基汞 胶质瘤 细胞增殖 细胞凋亡 Brain neuroglioma Methyl-mercuric chloride Apoptosis Morphology
  • 相关文献

参考文献7

  • 1陈儇,范茹军,毕晓颖,李志超.氯化甲基汞抗大鼠C6胶质瘤细胞的体外研究[J].吉林大学学报(医学版),2007,33(2):215-218. 被引量:8
  • 2Deorah S, Lynch CF, Sibenaller ZA, et al. Trends in brain cancer incidence and survival in the United States:Surveillance, Epidemiology, and End Results Program, 1973 to 2001[J]. Neurosurg Focus,2006 ;20 ( 4 ) : E1.
  • 3Pulkkanen K J, Yla-Herttuala S. Gene therapy for malignantglioma : current clinical status[ J]. Mol Ther,2005 ; 12 (4) :585-98.
  • 4Rosenthal MA, Kavar B, Uren S, et al, Promising survival in patients with high-grade gliomas following therapy with a novel boronated porphyrin [ J]. J Clin Neurosci ,2003 ; 10 (4) :425-7.
  • 5Mirlmanoff RO, Gorlia T, Mason W, et al. Radiotherapy and temozolomide for newly diagnosed glioblastoma: recursive partitioning analysis of the EORTC 26981/22981-NCIC CE3 phase Ⅲ randomized trial[ J]. J Clin Oncol, 2006 ; 24 ( 16 ) : 2563-9.
  • 6Berlin M. Neurotoxicity of methyhnercury in squirrel monkeys [ J]. Arch Environ Health, 1975 ; 30 ( 6 ) : 340 -34.
  • 7谢皓雪,张琨,崔贞玉,宋昕恬,吴小刚.氯化甲基汞及三氧化二砷对K562细胞凋亡的影响[J].中国卫生工程学,2008,7(5):257-258. 被引量:1

二级参考文献18

  • 1卢香兰,王萍萍,刘云鹏,李霞,侯科佐,刘静,岳瑶.三氧化二砷对人白血病细胞株NB4和K562及MOLt4的增殖、周期及凋亡的影响[J].肿瘤防治杂志,2004,11(6):586-588. 被引量:8
  • 2张适,张悦,毕晓颖,张鹏宇,陈小平,李志超.氯化三乙基锡对大鼠C6胶质瘤细胞增殖抑制作用[J].吉林大学学报(医学版),2006,32(2):234-237. 被引量:5
  • 3[1]Atchison WD,Hare MF.Mechanisms of methyl mercury-induced neurotoxicity[J].Faseb J,1994,8:622-629.
  • 4[2]Ying CO,Sally AT,Sandy CK,et al.Induction of growth arrest and DNA damage-inducible genes Gadd45 andGadd53 in primary.rodent embryonic cells following exposure to methylmercury[J].Toxicol App Pharmacol,1997,147:31 -38.
  • 5[3]Charles PC,Kim CN,Fang GF,et al.Arsonic induces apoptosis of multidrug-resistant human myeloid leukemia cells that express bcl-abl or over express mdr,mrp,bcl-2 or bcl-xl[J].Blood,2000,95(3):1014-1022.
  • 6[4]Chen GQ,Zhu J,Shi XG,et al.In vitro studies on cellular and molecular mechanisms of arsenic trioxide(As2O3) in the treatment of acute promyelocytic leukemia:induces K562 cell apoptosis with down regulation of BCL-2-Express and modulation of PML-RARa/PML protema[J].Blood,1996,3:1052.
  • 7[6]Yin T,Wu YL,Sun HP,et al.Combined effects of as 4S4 and im atinib on chronic myeloid leukemia cells and BCR-ABL oncoprotein[J].Blood,2004,104(13):4219-4225.
  • 8Limke TL,Atchison WD.Acute exposure to methylmercury opens the mitochondrial permeability transition pore in rat cerebellar granule cells[J].Toxicol Appl Pharmacol,2002,178 (1):52-61.
  • 9Ou YC,Thompson SA,Ponce RA,et al.Induction of the cell cycle regulatory gene p21 (Waf1,Cip1) following methylmercury exposure in vitro and in vivo[J].Toxicol Appl Pharmacol,1999,157 (3):203-212.
  • 10Ou YC,Thompson SA,Kirehner SC,et al.Induction of growth arrest and DNA damage-inducible genes Gadd45 and Gadd153 in primary rodent embryonic cells following exposure to methylmercury[J].Toxicol Appl Pharmacol,1997,147 (1):31-38.

共引文献7

引证文献1

二级引证文献2

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