Background This study aimed to investigate the effect of pcDNA3.1-vascular endothelial growth factor （VEGF）165 vector on vertebral cartilage endplate vascular buds and intervertebral discs. Methods Rabbits were rand...Background This study aimed to investigate the effect of pcDNA3.1-vascular endothelial growth factor （VEGF）165 vector on vertebral cartilage endplate vascular buds and intervertebral discs. Methods Rabbits were randomly assigned to the control and experimental groups with 10 in each. In the experimental group, we anesthetized the rabbits and exposed the front vertebral body. Using the mark of the longitudinal ossature of the front vertebral body of the lumbar vertebrae, we advanced a needle at the central point of the front fourth and fifth lumbar intervertebral discs and injected 20 pl pcDNA3.1-VEGF165. Similarly, in the control group, we injected 20 IJl pcDNA3.1. At 4 and 8 weeks post-injection, we examined the changes of the vertebral cartilage endplate using X-ray radiograph, histology, and scanning electron microscopy. Results The vertebral cartilage endplate calcification and degeneration in the experimental group were less than those in the control group at 8 weeks post-operation. The average number and diameter of vascular buds obviously increased in the experimental group at 4 and 8 weeks post-operation. The number of vascular buds and the diameter in the region of the inner annulus increased when compared to those in the area near the nucleus pulposus. Conclusions The pcDNA3.1-VEGF165 plasmid can increase the average number and diameter of vascular buds and decelerate intervertebral disc degeneration.展开更多
基金This study was supported by a grant from the National Natural Science Foundation of China，the Anhui Province Education Department Key Fund Project
文摘Background This study aimed to investigate the effect of pcDNA3.1-vascular endothelial growth factor （VEGF）165 vector on vertebral cartilage endplate vascular buds and intervertebral discs. Methods Rabbits were randomly assigned to the control and experimental groups with 10 in each. In the experimental group, we anesthetized the rabbits and exposed the front vertebral body. Using the mark of the longitudinal ossature of the front vertebral body of the lumbar vertebrae, we advanced a needle at the central point of the front fourth and fifth lumbar intervertebral discs and injected 20 pl pcDNA3.1-VEGF165. Similarly, in the control group, we injected 20 IJl pcDNA3.1. At 4 and 8 weeks post-injection, we examined the changes of the vertebral cartilage endplate using X-ray radiograph, histology, and scanning electron microscopy. Results The vertebral cartilage endplate calcification and degeneration in the experimental group were less than those in the control group at 8 weeks post-operation. The average number and diameter of vascular buds obviously increased in the experimental group at 4 and 8 weeks post-operation. The number of vascular buds and the diameter in the region of the inner annulus increased when compared to those in the area near the nucleus pulposus. Conclusions The pcDNA3.1-VEGF165 plasmid can increase the average number and diameter of vascular buds and decelerate intervertebral disc degeneration.
