放射性药物与Egr-Endostatin重组质粒的协同抑瘤作用 |
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引用本文: | 李勇,高慧棋,马铎,徐岩松,孙淑芳,杨志杰.放射性药物与Egr-Endostatin重组质粒的协同抑瘤作用[J].中国实验诊断学,2010,14(6):824-827. |
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作者姓名: | 李勇 高慧棋 马铎 徐岩松 孙淑芳 杨志杰 |
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作者单位: | 哈尔滨医科大学附属第一医院,PET-CT室,黑龙江,哈尔滨,150001 |
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基金项目: | 黑龙江省教育厅资助项目,黑龙江省卫生厅资助项目 |
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摘 要: | 目的探讨Egr-内皮抑素基因联合放射性药物-胶体32P对于大鼠肝癌的抑制效果。方法经局部引入基因重组质粒及胶体32P后于,7 d1、4 d2、1 d分别测肝癌的生长率,第21d测定肝癌微血管密度(MVD)、肿瘤细胞凋亡指数(AI)等指标的变化。结果各干预组的肿瘤体积生长率、MVD、AI与对照组指标相比均具有统计学差异,P均0.05-0.01,在所有干预组中,32P+Egr-Endostatin组的抑瘤效果最好,P均0.05-0.01。肝癌生长率方面,第7 d-14d,32P干预组与单纯内皮抑素基因组、Egr-内皮抑素基因组相比抑瘤效果相近,P0.05;但到达21 d时,胶体32P干预组治疗效果则明显下降。基因联合胶体32P的干预组效果均好于其它干预组,P0.05-0.01。MVD方面,32P组与其它干预组比较具有统计学差异,P0.01。AI指标,其他干预组与32P组比较具有差异,P0.05。结论 32P联合Egr-Endostatin基因协同抑瘤,可以发挥放射性药物的照射作用,Eg-1的辐射诱导增强作用及Endostatin基因的抑制肿瘤新生血管的三重作用,疗效最为确切。
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关 键 词: | 基因治疗 肝肿瘤 实验性 疾病模型 动物 大鼠 Wistar |
Radioactive Drugs and Egr-endostatin Synergistic Antitumor Effect |
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Institution: | LI Yong, GAO Hui-qi, MA Duo, et al. ( Department of PET - CT, the Affiliated First hospital of Harbin Medical University, Harbin 150001, China ) |
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Abstract: | Objective To investigate the antitumor effect of Egr-Endostatin gene combined with radioactive drug - colloidal I inhibitory on the rat liver. Methods After gene and colloidal 32 p were injected into liver cancer, the growth rate of liver cancer were measured at 7 d, 14 d, 21 d . Microvessel density determination (MVD)and apoptosis index (A I) were be measured at 21 d. Results Compared with the control the indexs in the treatment groups bad significant difference index( P 〈 0.05 - 0.01 ). The inhibitory effect of ^32 p + Egr-Endostatin is the best( P 〈 0.01 ). In the term of liver cancer growth rate, there are not significant difference between the ^32p group, Endostatin gene and Egr-Endostatin gene group in antitumor effect at 7 d - 14 d, ( P 〉 0.05) ; But at 21 d, the treatment effect of ^32 p group is clearly down. In terms of MVD, compared with the control group the treatment group has obvious statistical difference ( P 〈 0.01 ) ; compared with the other treatment group,^32p group has statistical difference( P 〈 0.01 ) ;^32 p + Endostatin group has statistical comparing with other groups( P 〈 0.01 ). In tems of AI index, the control group has statistical difference comparing with treatment groups ( P 〈 0.01 ) ;^32p group also has difference comparing with Endostatin group and Egr-Endostatin group ( P 〈 0.05) ; AI index of ^32 p + Endostatin group and ^32 p + Egr-Endostatin is better than other treatment groups( P 〈 0.05 - 0.01 ). Conclusion Colloidal ^32 p combining Egr-Endostatin gene plays the important role in treating liver cancer. ^32p can create the radiation function, Egr-1 can induce expression enhancement of Endostatin and the Endostatin Gene can inhibit liver ttanor angiogenesis. Therefore the whole effect of the three factors can manifestly decrease the liver cancer growing. |
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Keywords: | Wistar |
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