~(125)I诱导大鼠脑内胶质瘤凋亡实验研究

目的研究125I诱导人脑胶质瘤细胞系SHG-44体内外凋亡的可能性及其机制。方法体外培养SHG-44细胞,采用流式细胞仪法检测125I诱导SHG-44细胞凋亡及对细胞周期影响,采用立体定向的方法建立大鼠脑内人胶质瘤模型,1周后经MRI检测后,于肿瘤区接种125I,2周后复查MRI检测肿瘤大小,3周后处死大鼠,取对照组及肿瘤周边组织及肿瘤组织行Bcl-2、p53免疫组织化学染色。结果SHG-44细胞接种1周,MRI示脑内形成实体瘤;125I可抑制肿瘤生长,诱导细胞凋亡,延长荷瘤鼠生长周期,抑制Bcl-2基因表达,促进p53蛋白表达。结论125I具有体内、外抑制SHG-44细胞增殖,诱导凋亡的作用;其诱导凋亡机制可能与抑制Bcl-2蛋白表达,促进p53蛋白表达有关。

Experimental study of glioma cell apoptosis induced by ~(125)I in rats

Objective To investigate the possibility and mechanism of inducing human glioma cell line, SHG-44, apoptosis with 125I. Methods SHG-44 glioma cells were cultured in vitro, the cell cycle and apoptosis induction by 125I were detected by flow cytometry. A rat intracranial human glioma model was established using stereotactic methods, and 125I implanted into the glioma area 1 week later after MRI scans, 2 weeks later after the implantation, the diameter of tumor were measured by MRI scans. The rats were killed after 3 weeks; Bcl-2 and p53 gene expressions were detected by immunohistological methods both in control and experiment groups. Results One week after the SHG-44 implantation, tumor was found by MRI scan. 125I could inhibit the glioma growth, induce apoptosis and prolong the life period of tumor-bearing rats. Induced by 125I, the Bcl-2 gene expression was restrained and p53 gene expression was promoted. Conclusion 125I can both inhibit the glioma growth and induce SHG-44 cell apoptosis both in vitro and in vitro, which may be related to the inhibition of Bcl-2 expression and promotion of p53 gene expression.