【摘要】 目的研究125I诱导人脑胶质瘤细胞SHG-44体内外凋亡的可能性及其对p16基因的影响。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,采用免疫组化的办法,检测125I治疗前后的p16蛋白表达改变,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行接种前后肿瘤大小检测,3周后处死大鼠,取对照组及肿瘤周边组织及肿瘤组织行p16蛋白的免疫组化染色。结果125I接种1周后核磁共振检查,脑内形成实体瘤;125I可以抑制肿瘤生长,诱导细胞凋亡,促进p16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促进p16蛋白表达有关。更多还原

【Abstract】 Objective To investigate the possibility and mechanism of ~ 125 I induced apoptosis in human glioma and the change of p16 gene expression. Methods Cultured shg-44 glioma cells in vitro. The cell cycle and apoptosis were detected by flow cytometry methods and TUNEL methods. Stereotactic methods was used to establish the rat intracranial glioma model. The MRI scans were performed 1 week after implantation and ~ 125 I was implanted in the glioma area. 2 weeks later the MRI scans were performed to measure the diameter of tumor after implantation. The rats were killed after 3 weeks,p16 gene expression were tested by immunohistological methods both in control and experiment group. Results ~ 125 I could inhibit the growth and induced apotosis. The p16 gene expression was promoted. Conclusion ~ 125 I can both inhibit the growth of glioma and induce apoptosis. The mechanism may be concern with the promotion of p16 gene expression.更多还原