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目的:研究脂膜微囊承载紫杉醇靶向性治疗大鼠颅内C6胶质瘤的机制。方法:建立大鼠C6胶质瘤动物模型12只,成瘤大鼠分为四组;注射LCM-Taxol组,注射LCM组,注射Taxol组及载瘤动物组,每组取一只在最后一次尾静脉注射相应药物后处死,获取大鼠脑组织标本,进行常规HE染色,油红O染色,观察LCM在肿瘤位点分布的特点;同时观察不同处理组大鼠的生存期。结果:油红O染色显示注射LCM-Taxol组,肿瘤区域有LCM聚集,胶质瘤明显坏死;而注射LCM组,肿瘤区域有LCM出现,但肿瘤区域无明显坏死;注射TAXOL组及载瘤动物组肿瘤区域无明显坏死;生存期结果示Taxol-LCM组生存期明显长于注射LCM组和注射Taxol组及载瘤动物组,而注射LCM组、注射Taxol组、单纯载瘤动物组生存期差异不明显。结论:LCM-Taxol可以承载药物靶向性聚集于颅内胶质瘤区域,并起到杀伤肿瘤的作用,明显延长了大鼠的生存期;而注射LCM组、注射Taxol组未能明显延长载瘤大鼠的生存期。
Objective: To study the mechanism of liposomal microcapsules carrying paclitaxel-targeted therapy for intracranial C6 glioma in rats. Methods: Twelve rat models of C6 glioma were established. Tumor-bearing rats were divided into four groups: LCM-Taxol injection group, LCM injection group, Taxol injection group and parental injection group, After tail vein injection, the rats were sacrificed and the brain tissue samples of rats were obtained. HE staining and oil red O staining were performed to observe the distribution of LCM in tumor sites. The survival of rats in different treatment groups was also observed. Results: Oil red O staining showed that the LCM-Taxol injection group had LCM accumulation in the tumor area and glioma necrosis. In the LCM injection group, there was LCM in the tumor area but no necrosis in the tumor area. The survival of Taxol-LCM group was significantly longer than that of LCM group and Taxol group and parental animal group, while the difference between LCM group, Taxol injection group and pure parental tumor group was not significant obvious. CONCLUSION: LCM-Taxol can target drug-targeted aggregation in the intracranial glioma region and play a role in killing the tumor, significantly prolonging the survival time of the rats. LCM-injected Taxol group did not significantly prolong the loading time Survival of tumor in rats.