论文部分内容阅读
目的 观察胶质瘤荷瘤大鼠在二甲基甲酰胺 (DMF)诱导分化治疗过程中C myc蛋白表达 ,并探讨其意义。方法 实验组Wistar荷瘤大鼠给予每天 2次腹腔注射DMF 5 70mg/kg体重 ,共 2周 ;对照组给予盐水注射。计数荷瘤大鼠生存时间。免疫组织化学链霉素抗生物素蛋白 过氧化物酶染色及计算机图像分析检测大鼠肿瘤组织C myc蛋白表达。 结果 实验组生存时间(3 6.3± 2 .7)d较对照组 (2 8.0± 2 .4)d明显延长 (P <0 .0 1)。大鼠C myc蛋白阳性表达平均百分率 ,对照组为 (77.62± 12 .11) % ;实验组肿瘤周边为 (2 3 .80± 13 .83 ) %、肿瘤中心为 (4 4 .0 2±2 1.5 8) % ;肿瘤周边与中心比较、肿瘤周边及中心分别与对照组比较 ,差异均有非常显著性 (P <0 .0 1)。结论 DMF诱导胶质瘤凋亡的机制与抑制肿瘤细胞C myc蛋白表达有关
Objective To observe the expression of C-myc in glioma-bearing rats induced by dimethylformamide (DMF) and to explore its significance. Methods Experimental Wistar mice were given intraperitoneal injection of DMF 5 70mg / kg body weight twice per day for 2 weeks. The control group was given saline injection. Tumor bearing rats were counted for their survival time. Immunohistochemical streptavidin - avidin peroxidase staining and computer image analysis to detect C - myc protein expression in rat tumor tissue. Results The survival time of the experimental group (3 6.3 ± 2 .7) d was significantly longer than that of the control group (2 8.0 ± 2. 4) d (P <0.01). The average percentage of positive expression of C-myc protein in rats was (77.62 ± 12.11)% in the control group, (23.8 ± 13.83%) in the experimental group and (44.02 ± 2. 1.58)%. Compared with the center of the tumor, the difference between the periphery and the center of the tumor and the control group was significant (P <0.01). Conclusion The mechanism of DMF induced glioma apoptosis is related to the inhibition of Cmyc protein expression in tumor cells