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.
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。