首页 | 本学科首页   官方微博 | 高级检索  
检索        

中药安迪粉针剂的放射增敏作用
引用本文:李勤,谢艳华,孙纪元,梁克明,张庆,王倩,王四旺.中药安迪粉针剂的放射增敏作用[J].华西药学杂志,2003,18(1):6-9.
作者姓名:李勤  谢艳华  孙纪元  梁克明  张庆  王倩  王四旺
作者单位:1. 陕西省肿瘤医院,陕西,西安,710061
2. 第四军医大学药物研究所,陕西,西安,710032
3. 第四军医大学西京医院,陕西,西安,710038
摘    要:目的 探讨安迪粉针剂(Andi)增强电离辐射生物学效应的作用机理。方法 以人食管癌细胞株(ECA l09)为观察对象,采用电镜、流式细胞仪分析、台盼兰染色等方法,分别观察对照、Andi、^60Co—γ线照射和Andi 照射4个组对ECA 109细胞的形态、细胞周期、细胞凋亡和坏死等的影响;并采用改良硫代巴比妥酸荧光法测定丙二醛(MDA);羟胺法测定超氧化物歧化酶(SOD)。结果 在乏氧条件下,Andi能引起ECA 109细胞坏死(P<0.05),并增加MDA含量(P<0.05);而Andi 照射组的作用比单用Andi和单纯照射明显增强(F=6.53,P<0.01);从Andi、照射、Andi照射3个组的光镜和电镜结果发现,ECA l09癌细胞明显变性、坏死、凋亡,但以Andi 照射组的改变更显著;电镜显示Andi组有较多ECA l09细胞存在糖原颗粒堆积。结论Andi可以引起乏氧ECA 109细胞的糖代谢障碍,增加细胞内自由基的产生,引起细胞坏死;Andi与^60Co—γ线合用能进一步促进乏氧细胞坏死,具有协同作用;Andi放射增敏作用的机理可能与其促进癌细胞内自由基产生或影响癌细胞糖代谢有关。

关 键 词:安迪粉针剂  中药  放射增敏作用  作用机制  丙二醛  超氧化物歧化酶  糖代谢障碍  自由基  电离辐射生物学效应
文章编号:1006-0103(2003)01-0006-04
修稿时间:2002年8月1日

Mechanism of radiosensitizing effect of Andi
LI Qin ,XIE Yan-hua ,SUN Ji-yuan ,LIANG Ke-ming ,ZHANG Qing ,WANG Qian ,WANG Si-wang Shaanxi Provicial Cancer Hospital,Xi'an ,China.Mechanism of radiosensitizing effect of Andi[J].West China Journal of Pharmaceutical Sciences,2003,18(1):6-9.
Authors:LI Qin  XIE Yan-hua  SUN Ji-yuan  LIANG Ke-ming  ZHANG Qing  WANG Qian  WANG Si-wang Shaanxi Provicial Cancer Hospital  Xi'an  China
Institution:LI Qin 1,XIE Yan-hua 2,SUN Ji-yuan 2,LIANG Ke-ming 3,ZHANG Qing 1,WANG Qian 1,WANG Si-wang 2 1 Shaanxi Provicial Cancer Hospital,Xi'an 710061,China,2 Institute of Materia Medical in the Fourth Military Medical University,Xi'an 710032,China,3 Xijing Hospital in the Fourth Military Medical University,Xi'an 710038,China
Abstract:OBJECTIVE To study the mechanism of radiosensitizing effect of Andi.METHODS Human esophageal carcinoma cell line (ECA 109) were treated with culture medium, Andi, radiation and Andi combined with radiation in 99.99% nitrogen,respectively.The cells' morphological variation was observed from electroscopy. The cells'distribution in cell cycle was checked via flow cytometer. Necrosis was surveyed by dint of trypan blue stain and microscopy. Intracellular MDA and SOD were detected with modified thiobarbituric acid(TBA) fluorescence spectrophotometry of lipoperoxides (LPO) and spectrophotometry of hydroxylamine. RESULTS Under the experimental condition,necrosis of hypoxic cells and increased intracellular MDA were caused by Andi (P<0.05). With radiation to hypoxic cells, Andi produced more necrotic cells ( F=6.53,P <0.05).Under optic microscopy and electroscopy, several cells with denaturalization, necrosis or apoptosis were observed in groups treated with Andi and/or radiation. More of these changed cell were discovered in the group treated by Andi combined with radiation.Some cells with amassed hepatin were displayed by electroscopy in group treated with Andi. CONCLUSION Andi cause obstacle of glycometabolism in ECA 109 cells. It is able to aggravate cell necrosis and to increase intracellular free radical produced by radiation on the hypoxic cells.Andi with radiation further increase necrotic cells and they have cooperative effects.The mechanism of Andi's radiosensitizing effect on hypoxia cell may correlate with increasing intracellular free radical or affected glycometabolism.
Keywords:Radiosensitization  Andi  Free radical  Glycometabolism  Necrosis  Mechanism
本文献已被 CNKI 维普 万方数据 等数据库收录!
设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号