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目的 观察苯乙酸钠 (Na PA)治疗 G42 2胶质瘤小鼠的肿瘤细胞变化 ,并探讨其作用机制。方法建立颅内型和肌肉型 G42 2胶质瘤荷瘤鼠模型 ,两种模型各分成 5组。其中 3组为实验组 ,分别予 12 0 0、80 0、40 0 m g/ kg· d的 Na PA治疗。另两组中一组为阳性对照组 ,用卡氮芥 (BCNU)治疗 ,一组为阴性对照组 ,给予生理盐水。两种动物模型于接种瘤细胞 2 4小时后开始用药。阳性对照组腹腔注射 BCNU(2 0 m g/ kg) 1次 ,实验组和阴性对照组分别皮下注射 Na PA和生理盐水 ,共 14天。用药结束后 ,观察颅内型荷瘤鼠的药物毒性反应、小鼠生存期、计算生存率 ,并观察各组胶质瘤组织的病理及超微结构变化。对肌肉型荷瘤鼠 ,测定瘤重抑制率。结果 用 Na PA治疗的荷瘤鼠生存期均有延长 ;Na PA对胶质瘤生长有浓度依赖性抑制作用 ;病理和电镜显示 Na PA治疗后胶质瘤细胞核分裂像减少 ,粗面内质网增多 ,细胞突起出现 ,表示瘤细胞出现分化趋势。结论 Na PA主要通过诱导胶质瘤细胞分化抑制肿瘤生长。
Objective To observe the changes of tumor cells in the treatment of G42 glioma mice by sodium phenyl acetate (Na PA) and to explore its mechanism. Methods The intracranial and muscular G42 2 glioma tumor-bearing mice models were established, and the two models were divided into 5 groups. Three of them were experimental groups, which were treated with Na PA alone at 120, 80, 0 and 40 0 m g / kg · d respectively. The other two groups in a group of positive control group, with Carnosine (BCNU) treatment, a negative control group, given saline. Two animal models of tumor cells inoculated 24 hours after the start of medication. The positive control group was intraperitoneally injected with BCNU (20 mg / kg) once, and the experimental group and the negative control group were subcutaneously injected with Na PA and saline for 14 days respectively. After treatment, the toxicity of intracranial tumor-bearing mice was observed, the survival of mice was observed, the survival rate was calculated, and the pathological and ultrastructural changes of glioma tissues were observed. On muscle-bearing mice, determination of tumor weight inhibition rate. Results The survival time of tumor-bearing mice treated with Na-PA was prolonged. Na PA inhibited the growth of glioma in a concentration-dependent manner. The pathological and electron microscopy showed that the mitotic figures of glioma decreased after treatment with Na-PA, Increased, cell protrusions appear, indicating that the trend of tumor cells differentiation. Conclusion Na PA mainly inhibits tumor growth by inducing glioma cell differentiation.