Abstract：
BACKGROUND: Spinal cord injury (SCI) is a central nervous system injury that is primarily traumatic and manifests as autonomic dysfunction below the level of injury. Our previous studies have found that zinc ions have important effects on the nervous system and nerve repair, promoting autophagy and reducing inflammatory responses. However, the role of zinc ions in vascular regeneration is unclear.
OBJECTIVE: We investigated the effect of zinc ions after spinal cord injury from the perspective of a hypoxic microenvironment, and elucidated the role of VEGF-A secreted by microglia for vascular regeneration after spinal cord injury, providing new ideas for the treatment of spinal cord injury.
RESULTS: Zinc promotes functional recovery after spinal cord injury by regulating VEGF-A secretion from microglia. On the one hand, VEGF-A secreted by microglia promotes angiogenesis through the PI3K/AKT/Bcl-2 pathway and improves the hypoxic microenvironment after spinal cord injury. On the other hand, VEGF-A secreted by microglia was positively correlated with platelet endothelial cell adhesion molecule-1 (CD31), and zinc could increase the association between microglia and blood vessels.
CONCLUSIONS: Zinc promoted microglia secretion of VEGF-A, increased vascular endothelial cell proliferation and migration through the PI3K/AKT/Bcl-2 pathway, and inhibited microglia apoptosis.
OBJECTIVE: We investigated the effect of zinc ions after spinal cord injury from the perspective of a hypoxic microenvironment, and elucidated the role of VEGF-A secreted by microglia for vascular regeneration after spinal cord injury, providing new ideas for the treatment of spinal cord injury.
RESULTS: Zinc promotes functional recovery after spinal cord injury by regulating VEGF-A secretion from microglia. On the one hand, VEGF-A secreted by microglia promotes angiogenesis through the PI3K/AKT/Bcl-2 pathway and improves the hypoxic microenvironment after spinal cord injury. On the other hand, VEGF-A secreted by microglia was positively correlated with platelet endothelial cell adhesion molecule-1 (CD31), and zinc could increase the association between microglia and blood vessels.
CONCLUSIONS: Zinc promoted microglia secretion of VEGF-A, increased vascular endothelial cell proliferation and migration through the PI3K/AKT/Bcl-2 pathway, and inhibited microglia apoptosis.
摘要：
背景：脊髓损伤（SCI）是一种中枢神经系统损伤，主要是创伤性的，表现为低于损伤水平的自主神经功能障碍。我们之前的研究发现锌离子对神经系统和神经修复有重要作用,促进自噬和减少炎症反应。然而,锌离子在血管再生中的作用尚不清楚。
目的：我们从缺氧微环境的角度研究了锌离子在脊髓损伤后的作用，并阐明了小胶质细胞分泌的VEGF-A在脊髓损伤后血管再生中的作用，为脊髓损伤的治疗提供新思路。
结果：锌通过调节小胶质细胞分泌VEGF-A促进脊髓损伤后功能恢复。一方面,小胶质细胞分泌的VEGF-A通过PI3K/AKT/Bcl-2通路促进血管生成，改善脊髓损伤后缺氧微环境。另一方面,小胶质细胞分泌的VEGF-A与血小板内皮细胞粘附分子-1(CD31)呈正相关,锌可以增加小胶质细胞和血管之间的联系。
结论：锌促进小胶质细胞分泌VEGF-A，通过PI3K/AKT/Bcl-2途径增加血管内皮细胞增殖和迁移，并抑制小胶质细胞凋亡。
目的：我们从缺氧微环境的角度研究了锌离子在脊髓损伤后的作用，并阐明了小胶质细胞分泌的VEGF-A在脊髓损伤后血管再生中的作用，为脊髓损伤的治疗提供新思路。
结果：锌通过调节小胶质细胞分泌VEGF-A促进脊髓损伤后功能恢复。一方面,小胶质细胞分泌的VEGF-A通过PI3K/AKT/Bcl-2通路促进血管生成，改善脊髓损伤后缺氧微环境。另一方面,小胶质细胞分泌的VEGF-A与血小板内皮细胞粘附分子-1(CD31)呈正相关,锌可以增加小胶质细胞和血管之间的联系。
结论：锌促进小胶质细胞分泌VEGF-A，通过PI3K/AKT/Bcl-2途径增加血管内皮细胞增殖和迁移，并抑制小胶质细胞凋亡。
