摘要
目的:探讨125I粒子组织间植入对小鼠Lewis肺癌细胞Egr-1基因及caspase-3蛋白表达的影响。方法:建立小鼠Lewis肺癌模型,治疗组在瘤体内植入2粒表面放射活性为9.25MBq的BT-125-I型125I籽源,对照组植入2粒无放射活性的空心籽源。治疗21天,记录小鼠的存活率;处死存活小鼠,计算肿瘤体积抑制率。对摘除的肿瘤组织进行常规病理学检查和免疫组织化学检测caspase-3蛋白的表达,RT-PCR方法检测瘤组织Egr-1基因的表达。结果:治疗21天,治疗组和对照组小鼠存活率分别为88.88%和70.59%,差别无统计学意义(P>0.05);肿瘤体积抑制率为71.12%。病理检查显示治疗组近粒子处肿瘤细胞变性坏死,对照组近粒子处可见存活肿瘤细胞。免疫组织化学显示治疗组caspase-3表达强度高于对照组(P<0.01)。RT-PCR结果显示治疗组Egr-1表达高于对照组(P<0.01)。结论:125I粒子组织间植入可以抑制小鼠Lewis肺癌生长,其作用可能是通过上调癌细胞Egr-1和caspase-3的表达、促进细胞凋亡而实现的。
Objective：To explore the influence of interstitial brachytherapy with ^125I seeds on caspase-3 and Egr-1 expressions of lewis lung carcinoma in C57BL mice. Methods：Lewis lung cell（LLC） was planted into model mice of C57BL and were divided into the treatment group （ n = 18 ） and the control group （ n = 17 ）. In each mouse of the treatment group, two BT-125-I Model ^1251 seeds with apparent activity of 9. 25 MBq were implanted into the tumor; whereas in each mouse of the control group two dummy seeds were implanted. The mice survival rates of both groups were recorded after 21 days. The tumor weights and dimensions of survived mice were measured, and the tumor volume inhibition rate was calculated. T-test was performed to compare differences of tumor weights and volumes between these two groups. Routine pathological slides of tumor tissue were observed under light microscope. The expression of caspase-3 was detected by immunohistochemical method and the expression of Egr-1 was detected by RT-PCR method. Results：The survival rates were 88. 88% in the treatment group and 70. 59% in the control group, the difference had no statistical significance（P 〉 0.05 ）. The tumor volume inhibition rate was 71.12%. Pathological examination showed degeneration and necrosis of cancer cell at the site nearby the seed in the treated group, but the tumor cells alive were still presented nearby the seed in the control group. The expressions of Caspase-3 and Egr-1 in the treated group were highter than those in the control group（P 〈 0. 01 ）. Conclusion ：The interstitial brachytherapy with ^125I seeds could significantly inhibit the growth of lewis lung cacinoma of mice. The possible mechanism may be that ^125I interstitial brachytherapy can enhance the expressions of Egr-1 and caspase-3, which could induce tumor cellular apoptosis.
出处
《临床肿瘤学杂志》
CAS
2008年第3期201-204,共4页
Chinese Clinical Oncology
