文章摘要
任海燕,胡汉华,乔慧瑛,汤建安,谢风莲,张敏芳.异常黑胆质肝癌移植模型大鼠Rho/Rock信号通路相关分子表达研究[J].,2018,(4):621-626
异常黑胆质肝癌移植模型大鼠Rho/Rock信号通路相关分子表达研究
Research of Expression of Moleculars Related to Rho/Rock Signaling Pathway in the Transplanted Hepatoma Rats Model with Abnormal Savda Syndrome
投稿时间:2017-10-01  修订日期:2017-10-24
DOI:10.13241/j.cnki.pmb.2018.04.005
中文关键词: 异常黑胆质证候  肝癌模型  Rho/Rock信号通路  异常黑胆质成熟剂(ASM)
英文关键词: Abnormal savda  Hepatoma rats model  Rho/Rock signaling pathway  Abnormal Savda Munziq(ASM)
基金项目:新疆维吾尔自治区自然科学基金项目(2015211C022)
作者单位E-mail
任海燕 新疆医科大学中心实验室电镜室 新疆 乌鲁木齐 830011 424732833@qq.com 
胡汉华 新疆医科大学中心实验室电镜室 新疆 乌鲁木齐 830011  
乔慧瑛 吴江区第一人民医院老年医学科 江苏 苏州 215200  
汤建安 新疆医科大学中心实验室电镜室 新疆 乌鲁木齐 830011  
谢风莲 新疆医科大学中心实验室电镜室 新疆 乌鲁木齐 830011  
张敏芳 新疆医科大学中心实验室电镜室 新疆 乌鲁木齐 830011  
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中文摘要:
      摘要 目的:探讨异常黑胆质证肝癌移植模型大鼠Rho/Rock信号通路相关分子的蛋白表达,诠释异常黑胆质肿瘤高发的分子生物学基础。方法:采用足底电击、干寒饲料、铁管制动等多种因素刺激21 d建立异常黑胆质证大鼠模型,在此基础上通过肝内注射walker-256瘤细胞建立异常黑胆质大鼠肝癌移植模型,观察其肝脏组织形态结构变化,并采用Western Blot法检测大鼠肝脏相关蛋白的表达变化。结果:异黑肿瘤组肝脏组织形成明显癌巢,与对照组相比癌旁组织肝索结构紊乱,癌细胞向肝小叶深部迁移;异常黑胆质成熟剂给药组癌细胞崩解、凋亡,胶原纤维增生,癌旁肝索重构。与对照组相比,肿瘤组Cdc42和Rock2蛋白表达均明显增加(P<0.05),异黑肿瘤组Cdc42、Rac1、Rock1、Rock2和Myl1蛋白表达明显增加(P<0.05);与异黑肿瘤组相比,异常黑胆质成熟剂(ASM)给药组Cdc42、Rac1、Rock1、Rock2和Myl1蛋白表达呈剂量依赖性降低(P<0.05),且与对照组无显著差异。结论:异常黑胆质证肝癌移植模型可能与Rho /Rock信号通路分子通过调控肌动蛋白收缩引起的肿瘤细胞侵袭、转移生物学行为等作用有关,异常黑胆质成熟剂可能通过下调Rho /Rock信号通路分子使损伤的组织形态逆转。
英文摘要:
      ABSTRACT Objective: To study the expression of moleculars related to Rho/Rock signaling pathway in the transplanted hepatoma rats model with abnormal savda syndrome and explain the molecular biology mechanism of high incidence of abnormal savda syndrome tumors. Methods: The rats model with abnormal savda syndrome were developed by electric shock, cold feeding, iron pipe braking and other factors for 21 days. Then the transplanted hepatoma rats model were established by inoculating walker-256 ascites tumor cells into the liver. At last the changes of morphological structure was observed and the expression of related proteins was detected by Western Blot method in rats' liver. Results: Compared with the control group, obvious tumor nests could be observed in the model with the abnormal savda syndrome group, the adjacent tissue of the cancer was disordered, the cancer cells migrated to the deep of hepatic lobule; Cancer cells disintegration and apoptosis、collagen proliferation、reconstruction of hepatic cord near cancer could be observed in the treatment group with ASM. Compared with the control group, the expression of Cdc42 and Rock2 proteins was significantly higher in the model control group(P<0.05), the expression of Cdc42, Rac1, Rock1, Rock2 and Myl1 proteins was significantly higher in the model with the abnormal savda syndrome group(P<0.05); Compared with the model with the abnormal savda syndrome group, the expression of Cdc42, Rac1, Rock1, Rock2 and Myl1 proteins showed dose-dependent decrease in the treatment group with ASM(P<0.05). Conclusion: There was certain correlation between the model with the abnormal savda syndrome and tumor cells invasion, transfer caused by moleculars related to Rho/Rock signaling pathway regulating actin contraction, ASM might reverse the injury of histomorphology through down-regulating the moleculars related to Rho/Rock signaling pathway.
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