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Physicochemical Properties of Musk Deer Pneumonia and Purulent Disease Viruses 被引量:1
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作者 LUO Yan KANG Ji-ping +5 位作者 CHENG Jian-guo ZOU Li-kou LIBei dai xiao-yang WANG Cheng-xu YU Guang-min 《Animal Husbandry and Feed Science》 CAS 2010年第5期37-40,共4页
[ Objective] To understand the physicochemical properties of musk deer pneumonia and purulent disease viruses. [ Method] The pneu- monia and purulent disease viruses were isolated from the abnormal and purulent lung t... [ Objective] To understand the physicochemical properties of musk deer pneumonia and purulent disease viruses. [ Method] The pneu- monia and purulent disease viruses were isolated from the abnormal and purulent lung tissues of musk deer. Then the isolated viruses were inocula- ted into the Vero cells. After culturing, the virus solution was collected and used to determine TCID50 and genoma types. The sensitivity to fat sol- vent, resistance to hydrochloric acid and trypsin as well as tolerance to heat of the musk deer pneumonia and purulent disease viruses were detec- ted, respectively. [ Result] The obvious cytopathic effects (CPE) were found in Veto cells infected by the isolated viruses. The virus was 2-1.43 TCID50/ml and its genome was RNA. The virus was not sensitive to chloroform, 1% trypsin and heats, and it had a certain tolerance to 0.1 mol/L hy- drochloric acid. [ Conclusion] The study on the physicochemical properties of musk deer pneumonia and purulent disease viruses lays a foundation for prevention and control of the musk deer pneumonia and purulent diseases. 展开更多
关键词 Musk deer Pneumonia and purulent disease viruses Physicochemical properties ISOLATION
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阿司匹林抑制HGF/c-Met介导的肿瘤细胞转移作用
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作者 代晓阳 陈思康 车金鑫 《药学学报》 CAS CSCD 北大核心 2022年第10期2985-2994,共10页
本研究主要探讨了阿司匹林对肝细胞生长因子/细胞间质表皮转化因子受体(HGF/c-Met)轴介导的肿瘤生物学效应的影响,初步探究阿司匹林抑制肿瘤转移的分子机制。利用分子模拟预测阿司匹林与c-Met的结合情况;采用蛋白质胞内热稳定性实验验... 本研究主要探讨了阿司匹林对肝细胞生长因子/细胞间质表皮转化因子受体(HGF/c-Met)轴介导的肿瘤生物学效应的影响,初步探究阿司匹林抑制肿瘤转移的分子机制。利用分子模拟预测阿司匹林与c-Met的结合情况;采用蛋白质胞内热稳定性实验验证阿司匹林在细胞水平与c-Met的结合情况;采用激酶活性检测阿司匹林对c-Met激酶的抑制作用;Western blot、细胞分散实验、细胞分枝形态变化实验及Transwell实验用于检测细胞信号转导、形态与迁移能力的变化。结果显示,阿司匹林能够有效抑制c-Met的激酶活性,半数抑制浓度为0.95 mmol·L^(-1)。分子模拟实验结果显示,阿司匹林能够结合在c-Met蛋白的ATP口袋,主要结合位点为Tyr1230、Tyr1159和Met1229。同样,蛋白质胞内热稳定性实验显示,阿司匹林能够与c-Met蛋白结合。Western blot结果显示,阿司匹林能够浓度依赖性地抑制HGF刺激后磷酸化Met的上调。细胞分散实验结果显示,阿司匹林能够浓度依赖性地阻断HGF/c-Met介导的细胞分散,在4 mmol·L^(-1)浓度下阿司匹林几乎可以完全阻断c-Met活化介导的生物学功能,且该阻断作用与HGF无关。同样,细胞分枝实验结果显示,阿司匹林能够浓度依赖性抑制HGF/c-Met介导的MDCK细胞侵袭性生长细胞分枝的形态变化。Transwell实验结果显示,阿司匹林能够浓度依赖性地阻断HGF/c-Met介导的细胞迁移与侵袭,在4 mmol·L^(-1)浓度下阿司匹林几乎可以完全阻断c-Met活化介导的生物学功能,且该阻断作用与HGF无关。以上结果表明,阿司匹林能够与c-Met结合,进而阻断HGF/c-Met介导的生物学效应,从而发挥抑制肿瘤转移的作用。本研究揭示了阿司匹林的新生物学功能,为全面理解阿司匹林的抗肿瘤转移作用提供了新的理论基础。 展开更多
关键词 阿司匹林 肿瘤转移 HGF/C-MET 受体酪氨酸激酶 小分子抑制剂
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