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Antitumor effect of curcumin liposome after transcatheter arterial embolization in VX2 rabbits

机译:Vx2兔经沟管动脉栓塞后姜黄素脂质体的抗肿瘤作用

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摘要

Background: Hypoxia may affect the therapeutic efficacy of transcatheter arterial embolization (TAE), which is widely used in nonsurgical hepatocellular carcinoma (HCC). Liposomal curcumin can exert anticancer effect. Our purpose is to explore the antitumor effect of liposomal curcumin on the HCC after TAE. Methods: The HepG2 cells were cultured under hypoxic condition (1% O-2) and then treated with curcumin liposome. Cell viability, apoptosis and cell cycle were respectively measured by CCK-8 and a flow cytometry. The VX2 rabbits were randomly distributed into three groups: control group with saline embolization, TAE group with lipiodol embolization and curcumin liposome group with curcumin liposome and lipiodol embolization. MRI and CT perfusion scanning were performed after embolization. The hepatocyte apoptosis was measured by the terminal deoxyribonucleotidyl transferse-mediated dUTP nick-end labelling (TUNEL). The vascular endothelial growth factor (VEGF) and microvessel density (MVD) were measured by immunohistochemical. RT-PCR and Western blot were performed to examine mRNA and protein levels. Results: By regulating the apoptosis-related molecules, curcumin liposome obviously inhibited the cell viability and promoted the apoptosis in G1 phase. Curcumin liposome reduced the tumor size and alleviated neoplasia in VX2 rabbits. Curcumin liposome decreased the expressions of MVD and VEGF and increased the apoptosis of liver tissues. The levels of hypoxia-inducible factor-1 alpha (HIF-1 alpha) and survivin were suppressed by curcumin liposome both in hypoxic cells and liver tissues in the VX2 rabbits. Conclusion: Curcumin liposome exerted antitumor effect by regulating the proliferation- and apoptosis-related molecules. Curcumin liposome suppressed the HIF-1 alpha and survivin levels and inhibited the angiogenesis in VX2 rabbits after TAE.
机译:背景:缺氧可能影响经转截管动脉栓塞(TAE)的治疗效果,其广泛用于非静脉肝细胞癌(HCC)。脂质体姜黄素可以发挥抗癌效果。我们的目的是在TAE之后探讨脂质体姜黄素对HCC的抗肿瘤作用。方法:HEPG2细胞在缺氧条件下培养(1%O-2),然后用姜黄素脂质体处理。细胞活力,细胞凋亡和细胞周期分别通过CCK-8和流式细胞术测量。将Vx2兔随机分为三组:用盐水栓塞的对照组,具有脂碘栓塞和姜黄素脂质体组,姜黄素脂质体和脂碘醇栓塞。在栓塞后进行MRI和CT灌注扫描。通过末端脱氧核糖核苷酸转孔介导的DURP缩乳末端标记(TUNEL)测量肝细胞凋亡。通过免疫组织化学测量血管内皮生长因子(VEGF)和微血管密度(MVD)。进行RT-PCR和Western印迹以检查mRNA和蛋白质水平。结果:通过调节凋亡相关的分子,姜黄素脂质体显然抑制细胞活力并促进了G1相中的凋亡。姜黄素脂质体在Vx2兔中减少了肿瘤大小和缓解肿瘤。姜黄素脂质体降低了MVD和VEGF的表达,并增加了肝组织的凋亡。通过姜黄素脂质体在Vx2兔中的缺氧细胞和肝组织中抑制缺氧诱导因子-1α和Survivin的水平。结论:姜黄素脂质体通过调节增殖和凋亡相关分子来施加抗肿瘤效果。姜黄素脂质体抑制了HIF-1α和Survivin水平,并在TAE之后抑制Vx2兔中的血管生成。

著录项

  • 来源
    《Cancer biology & therapy》 |2019年第6期|共11页
  • 作者单位

    Nanjing Med Univ Affiliated Canc Hosp Jiangsu Inst Canc Res Dept Radiol Jiangsu Canc Hosp 42;

    Second Hosp Nanjing Dept Intervent Nanjing Jiangsu Peoples R China;

    Nanjing Med Univ Affiliated Canc Hosp Jiangsu Inst Canc Res Dept Intervent Jiangsu Canc Hosp;

    Nanjing Med Univ Affiliated Canc Hosp Jiangsu Inst Canc Res Dept Radiol Jiangsu Canc Hosp 42;

    Nanjing Med Univ Affiliated Canc Hosp Jiangsu Inst Canc Res Dept Radiotherapy Jiangsu Canc Hosp;

    Nanjing Med Univ Affiliated Canc Hosp Jiangsu Inst Canc Res Dept Radiol Jiangsu Canc Hosp 42;

    Nanjing Med Univ Affiliated Canc Hosp Jiangsu Inst Canc Res Dept Radiol Jiangsu Canc Hosp 42;

    Nanjing Med Univ Affiliated Canc Hosp Jiangsu Inst Canc Res Dept Radiol Jiangsu Canc Hosp 42;

  • 收录信息
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 肿瘤学;
  • 关键词

    curcumin liposome; hypoxia; TAE; liver tumor; HIF-1 alpha; angiogenesis; antitumor;

    机译:姜黄素脂质体;缺氧;TAE;肝肿瘤;HIF-1α;血管生成;抗肿瘤;

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