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作 者:张璐璐[1,2] 张维东[1] 武力存 张月英[1] 王兆朋[1] 王朝霞[1] 贾青[1] 赵嵌嵌[1,2]
机构地区:[1]山东省医学科学院基础医学研究所病理室,山东省罕见病重点实验室,山东济南250062 [2]济南大学山东省医学科学院医学与生命科学学院,山东济南250062
出 处:《中草药》2015年第8期1190-1194,共5页Chinese Traditional and Herbal Drugs
基 金:国家自然科学基金资助项目(81073102;30873408);国家自然科学基金青年基金项目(81403150);山东省自然科学基金资助项目(ZR2010HQ003);国家青年科学基金项目(81303077)
摘 要:目的探讨蝎毒多肽提取物(polypeptide extract from scorpion venom,PESV)抑制S180肉瘤的机制。方法小鼠30只,建立S180肉瘤皮下荷瘤模型,随机分为对照组、PESV组和雷帕霉素(rapamycin,RAPA)组,每组10只,给药组ig给药,连续给药14 d。绘制肿瘤体积生长曲线并且计算抑瘤率;HE染色观察各组肿瘤组织病理变化;免疫组织化学法检测肿瘤组织中Beclin1、MAP1LC3A、CD133的蛋白表达差异;Western blotting检测各组肿瘤组织中Beclin1、MAP1LC3A、CD133的蛋白表达。结果 PESV组和RAPA组移植瘤的生长受到明显抑制,PESV组与RAPA组的抑瘤率分别为17.9%和25.0%(P<0.05)。与对照组相比,PESV组和RAPA组Beclin1、MAP1LC3A蛋白表达明显上调(P<0.05)。且CD133的蛋白表达明显下调(P<0.01)。结论 PESV可抑制S180肉瘤细胞生长,其机制可能与促进自噬相关因子Beclin1、MAP1LC3A的表达及抑制肿瘤干细胞标志物CD133的表达有关。Objective To explore the inhibitory mechanism of polypeptide extract from scorpion venom(PESV) on sarcoma S180. Methods Thirty mice were implanted with S180 cells and randomly divided into three groups: control group, PESV group, and rapamycin(RAPA) group with 10 mice in each group. Then the tumor volume growth curve was drawn and the tumor inhibitory rate(IR) was calculated. The morphological changes of the tumor tissue were observed by HE staining. The protein expression levels of Beclin1, MAP1LC3 A, and CD133 were detected using immunohistochemical assay. Western blotting was applied to detecting the expression of Beclin1, MAP1LC3 A, and CD133 in tumor tissue of mice in each group. Results The growth of sarcoma S180 transplanted tumor was inhibited more obviously in the PESV group and RAPA group than that in the control group. The IR in the PESV and RAPA groups were 17.9% and 25.0%, respectively(P〈0.05). Compared with the control group, the protein expression of Beclin1 and MAP1LC3A increased while the protein expression of CD133 decreased(P〈0.05). Conclusion PESV can inhibit the growth of sarcoma S180, the mechanisms might be associated with promoting the expression of autophagic relative factors, Beclin1 and MAP1LC3 A as well as inhibiting the expression of CD133.
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