文章摘要
任海燕,张敏芳,朱虎虎,谢风莲,汤建安,胡汉华.ASM对异常黑胆质肝癌移植大鼠模型的干预[J].,2018,(8):1457-1462
ASM对异常黑胆质肝癌移植大鼠模型的干预
Intervention of ASM on the Transplanted Hepatoma Rats Model with Abnormal Savda Syndrome
投稿时间:2017-10-07  修订日期:2017-10-30
DOI:10.13241/j.cnki.pmb.2018.08.011
中文关键词: 异常黑胆质  肝癌大鼠模型  异常黑胆质成熟剂(ASM)
英文关键词: Abnormal savda  Hepatoma rats model  Abnormal Savda Munzip(ASM)
基金项目:国家自然科学基金项目(81360569)
作者单位E-mail
任海燕 新疆医科大学中心实验室 新疆 乌鲁木齐 830011 424732833@qq.com 
张敏芳 新疆医科大学中心实验室 新疆 乌鲁木齐 830011  
朱虎虎 新疆医科大学动物实验中心 新疆 乌鲁木齐 830011  
谢风莲 新疆医科大学中心实验室 新疆 乌鲁木齐 830011  
汤建安 新疆医科大学中心实验室 新疆 乌鲁木齐 830011  
胡汉华 新疆医科大学中心实验室 新疆 乌鲁木齐 830011  
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中文摘要:
      摘要 目的:探讨移植法制备异常黑胆质肝癌模型的可行性及维药异常黑胆质成熟剂(ASM)对肿瘤的干预作用。方法:用随机法将雄性SD大鼠分为正常对照组、模型对照组、病症模型组以及ASM药物治疗组(低、中、高剂量),正常对照组行假肝癌移植术(肝内注射生理盐水);模型对照组采用移植法将walker-256腹水瘤细胞进行肝内接种,建立肝癌模型;病症模型组首先采用多重因素(干寒饲养、足底刺激、铁管制动等)诱导制备异常黑胆质证大鼠模型,在此基础上进行肝内接种walker-256腹水瘤细胞,建立异常黑胆质证肝癌大鼠模型;ASM药物治疗组分为低、中、高不同剂量组(2.53, 5.06, 10.12 g/kg),异常黑胆质证大鼠接种瘤细胞后给予ASM灌胃治疗。2 w后处死取材,观察各组大鼠肿瘤发生情况、肿瘤体积、腹水形成率及腹壁后转移率;通过光镜及电镜观察各组大鼠肝癌组织肿瘤细胞形态结构变化。结果:模型对照组与病症模型组大鼠在肿瘤发生率、腹壁后转移率及肿瘤体积大小方面无显著差异(P>0.05);与模型对照组相比,病症模型组大鼠腹水形成率显著增高,差异有统计学意义(P<0.05);与病症模型组相比,低、中剂量ASM可以显著减小肿瘤体积、降低腹水形成率及腹壁后转移率(P<0.05),而高剂量ASM组仅有腹水形成率显著降低(P<0.05),肿瘤体积及腹壁后转移率无明显变化;光镜及电镜下观察可见,不同剂量ASM治疗组大鼠肿瘤细胞的水肿程度增加,瘤细胞发生变性坏死,其周围炎性细胞浸润明显增多。结论:异常黑胆质可能促进肝癌腹水形成和转移,从而影响肝癌的发展及转归;ASM对肿瘤细胞有一定损伤,可以减少肝癌腹水形成和转移,从而起到一定的抗肿瘤作用,影响肿瘤转归。
英文摘要:
      ABSTRACT Objective: To study the feasibility of the establishment of the transplanted hepatoma rats model with abnormal savda syndrome and evaluate the intervention of Abnormal Savda Munziq(ASM). Methods: The rats were divided into the control group, the model control group, the model with the abnormal savda syndrome group and the treatment group with ASM(2.53, 5.06, 10.12 g/kg). The transplanted hepatoma rats model was established by inoculating walker-256 ascites tumor cells into the liver. The model rats with abnormal savda syndrome was first established by using multi-complicated induced methods for 3 weeks, such as electric shock, cold feeding environment and iron pipe braking, etc, then were inoculated the walker-256 ascites tumor cells into the liver. The treatment groups were administrated with the ASM 2.53, 5.06, 10.12 g/kg for two weeks after the rats model with abnormal savda syndrome has injected tumor cells. The tumor incidence, tumor size, the ascites formation rate and abdominal metastatic rate were calculated and the tumor cell morphological structure changes were observed under the light microscope and electron microscope. Results: Between the model control group and the model with the abnormal savda syndrome group, there were no statistical significance in the tumor incidence, abdominal metastatic rate and tumor size (P>0.05), but compared with the model control group, the ascites formation rate was significantly higher in the model with the abnormal savda syndrome group(P<0.05); Compared with the model with abnormal savda syndrome, there were obvious decrease of tumor size, the ascites formation rate and abdominal metastatic rate in the treatment group with ASM(2.53, 5.06 g/kg), and there was only significantly decrease of the ascites formation rate in 10.12 g/kg ASM. Under the light microscope and electron microscope, we found edema degree of tumor cell aggravated, necrosis tumor cells and infiltrated inflammatory cells increased in the groups of ASM. Conclusion: Abnormal savda may promote the formation of ascites and metastasis of liver cancer, then affect the development and outcome of liver carcinoma; ASM has a certain anti-cancer effect and improve tumor outcome through demaging tumor cells and reducing ascites and metastatic.
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