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中文摘要：
活血化瘀药既抑制肿瘤血管生成，又促进心肌缺血的血管生成，临床皆有重要价值，其机制未明，困惑颇多。最新研究发现分别存在于尖端细胞和柄细胞上的两个配体DLL4与Jagged1对出芽式血管生成的调控存在交互平衡的作用，并且在肿瘤缺氧微环境中该平衡被打破。结合我们前期有关川芎及丹参有效成分对于血管芽生的研究，推测影响DLL4与Jagged1对肿瘤出芽式血管生成的调控可能是活血化瘀药抗肿瘤转移的新机制。本项目采用缺氧诱导的斑马鱼血管芽生模型，体外采用三维肿瘤血管生成的仿真模型，结合分子生物学手段，可视、动态地观察活血化瘀药对缺氧微环境下肿瘤血管的结构、功能、血管生成过程的影响，探讨其对血管尖端细胞DLL4与柄状细胞Jagged1的表达和血管芽生的关系。本课题试图揭示活血化瘀药在不同病理状态下表现为促进或抑制血管生成的科学内涵，为指导临床用药提供科学依据。
英文摘要：
Huo Xue Hua Yu drugs；luminescence tumor；sprouting angiogenesis；DLL4/Jagged1；Notch
结论摘要：
活血化瘀药既抑制肿瘤血管生成，又促进心肌缺血的血管生成，临床皆有重要价值，其机制未明，困惑颇多。最新研究发现分别存在于尖端细胞和柄细胞上的两个配体DLL4与Jagged1对出芽式血管生成的调控存在交互平衡的作用，并且在肿瘤缺氧微环境中该平衡被打破。结合我们前期有关川芎及丹参有效成分对于血管芽生的研究，推测影响DLL4与Jagged1对肿瘤出芽式血管生成的调控可能是活血化瘀药抗肿瘤转移的新机制。本项目采用缺氧诱导的斑马鱼血管芽生模型，体外采用三维肿瘤血管生成的仿真模型，结合分子生物学手段，可视、动态地观察活血化瘀药对缺氧微环境下肿瘤血管的结构、功能、血管生成过程的影响，探讨其对血管尖端细胞DLL4与柄状细胞Jagged1的表达与血管芽生的关系。本课题试图揭示活血化瘀药在不同病理状态下表现为促进或抑制血管生成的科学内涵，为指导临床用药提供科学依据。
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CryptotanshinoneActivates p38/JNK and Inhibits Erk1/2 Leading to Caspase-Independent Cell Deathin Tu
Luteolin reduces theinvasive potential of malignant melanoma cells by targeting β3 integrin and thee
Inhibition of hypoxia-induced epithelialmesenchymal transition by luteolin in non-small cell lung ca
The Angiogenic Responses Induced by Release of AngiogenicProteins from Tumor Cell-Activated Platelet
Cryptotanshinone, a novel tumor angiogenesisinhibitor, destabilizes tumor necrosis factor-a mRNA via
Chemopreventive efficacy of menthol on carcinogen-induced cutaneous carcinoma in mice throughinhibit
Holothurian glycosaminoglycan inhibits metastasis via inhibition of P-selectin in B16F10 melanoma ce
PKM2 Regulates Hepatocellular Carcinoma Cell Epithelial-mesenchymal Transition and Migration upon EG
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Phenolcarboxylic acids from medicinal herbs exert anticancer effects through disruption of COX-2 act
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