荷非小细胞肺癌裸鼠体内~(131)I-17-AAG的分布及其抗癌潜力

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目的:探讨131I-17-丙基胺基-17-去甲氧基格尔德霉素(131I-17-AAG)在荷瘤裸鼠体内的生物学分布及其抗癌机制。方法:通过不同给药方式(131I-17-AAG间质给药或静脉给药、Na131I间质给药对照及竞争性显像),显像比较12只模型鼠体内分布情况,每只5.55MBq0.1mL。1周后处死取瘤,电镜和免疫组化检测细胞凋亡和Ki-67、Bcl-2蛋白表达情况,设空白对照组(n=3)。另取24只,分别通过间质或尾静脉注射131I-17-AAG(每只1.85MBq0.1mL),不同时间处死,取血并测主要组织脏器的放射性计数率值。结果:显像提示,间质注射131I-17-AAG瘤体内放射性浓聚并长时间滞留,体内分布实验进一步证实;尾静脉给药瘤体内存在一定放射性摄取,药物体内清除较快;Na131I注射后迅速排出体外,无瘤内滞留;竞争性显像示瘤内摄取降低。电镜观测给药组较对照组肿瘤增长抑制显著。Bcl-2和Ki-67阳性表达率131I-17-AAG给药组要低于对照组。不同给药组组间比较及与对照组比较差异有统计学意义,Pmax=0.004。结论:131I-17-AAG间质给药在瘤组织内有明确药代学分布和药效学作用,可行进一步肿瘤治疗研究。 Objective: To investigate the biological distribution of 131I-17-propylamino-17-demethoxygeldanamycin (131I-17-AAG) in tumor-bearing nude mice and its anticancer mechanism. Methods: The distribution of 12 models of mice was compared by different administration modes (131I-17-AAG interstitial administration or intravenous administration, Na131I interstitial administration control and competitive imaging), each 5.55MBq0 .1 mL. One week later, the tumor was sacrificed and the apoptosis and expression of Ki-67 and Bcl-2 were detected by electron microscopy and immunohistochemistry. The blank control group (n = 3) was established. Twenty-four other mice were sacrificed at different times by 131I-17-AAG (1.85MBq0.1mL) injected into the interstitium or caudal vein. The blood was taken and the radioactivity count of the major organs was measured. Results: Imaging showed that radioactive accumulation of 131I-17-AAG tumor in the interstitium and long-term accumulation in vivo were further confirmed by in vivo distribution experiments. Some radioactive uptake into the tail vein was observed in the tumor tissue, Rapidly excreted, tumor-free retention; competitive imaging showed decreased intra-tumor. Electron microscope observation group than the control group tumor growth was significantly inhibited. The positive expression rate of Bcl-2 and Ki-67 in 131I-17-AAG group was lower than that in control group. The difference between the two groups was statistically significant, Pmax = 0.004. Conclusion: 131I-17-AAG interstitial drug delivery in the tumor tissue has a clear pharmacokinetic distribution and pharmacodynamic effects, further research on the treatment of cancer.
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