Department of Cell Biology, China Medical University, Shenyang, Liaoning 110122, P.R. China.
Department of Cardiac Surgery, First Hospital of China Medical University, Shenyang, Liaoning 110122, P.R. China.
Mol Med Rep. 2017 Oct;16(4):4455-4462. doi: 10.3892/mmr.2017.7169. Epub 2017 Aug 4.
Angiogenesis is an important process in the pathogenesis of aortic aneurysm. The aim of the present study was to investigate the angiogenic balance and the expression of vascular endothelial growth factor (VEGF) in thoracic aortic aneurysm (TAA). A previous study demonstrated that curcumin exerts a marked effect on aortic aneurysm development. Therefore, the present study determined whether curcumin is able to modulate angiogenesis and inflammatory signaling in TAA by collecting human TAA samples and establishing a rat TAA model using periaortic application of CaCl2. TAA rats were treated with curcumin or 1% carboxymethyl cellulose and were sacrificed 4 weeks after the operation. All tissue specimens were analyzed by histological staining, immunohistochemistry and western blotting. Human TAA samples exhibited increased neovascularization and VEGF expression when compared with normal aortic walls. In rat tissues, treatment with curcumin resulted in reduced aneurysm size and restored the wavy structure of the elastic lamellae. In addition, curcumin decreased neovascularization and the expression of VEGF. Immunohistochemical analysis indicated that curcumin significantly inhibited infiltration of cluster of differentiation (CD)3+ and CD68+ cells in TAA. Furthermore, curcumin treatment decreased the expression of vascular cell adhesion molecule‑1, intracellular adhesion molecule‑1, monocyte chemoattractant protein‑1 and tumor necrosis factor‑α. Collectively, the results demonstrated that angiogenesis and VEGF expression were increased in the aortic wall in TAA. Treatment with curcumin inhibited TAA development in rats, which was associated with suppression of VEGF expression. In addition, curcumin attenuated inflammatory cell infiltration and suppressed inflammatory factor expression in the periaortic tissue of TAA.
血管生成是主动脉瘤发病机制中的一个重要过程。本研究旨在探讨胸主动脉瘤(TAA)中的血管生成平衡和血管内皮生长因子(VEGF)的表达。先前的研究表明姜黄素对主动脉瘤的发展有显著作用。因此,本研究通过收集人 TAA 样本并使用氯化钙进行主动脉旁应用建立大鼠 TAA 模型,确定姜黄素是否能够调节 TAA 中的血管生成和炎症信号。TAA 大鼠用姜黄素或 1%羧甲基纤维素处理,并在手术后 4 周处死。所有组织标本均通过组织学染色、免疫组织化学和 Western blot 进行分析。与正常主动脉壁相比,人 TAA 样本显示出增加的新生血管形成和 VEGF 表达。在大鼠组织中,姜黄素治疗导致动脉瘤体积减小,并恢复弹性层的波浪状结构。此外,姜黄素降低了新生血管形成和 VEGF 的表达。免疫组织化学分析表明,姜黄素可显著抑制 TAA 中 CD3+和 CD68+细胞的浸润。此外,姜黄素治疗降低了血管细胞黏附分子 1、细胞间黏附分子 1、单核细胞趋化蛋白 1 和肿瘤坏死因子-α的表达。综上所述,这些结果表明 TAA 主动脉壁中的血管生成和 VEGF 表达增加。姜黄素治疗抑制了大鼠 TAA 的发展,这与 VEGF 表达的抑制有关。此外,姜黄素减轻了 TAA 主动脉旁组织中炎症细胞浸润和炎症因子的表达。