[Nrp-1 expression in healing process of traumatic brain injury combined with tibial fracture].

ABSTRACT

OBJECTIVE: To examine the expression of neuropilin-1 (Nrp-1), semaphorin 3A (Sema3A) and vascular endothelial growth factor (VEGF) in the healing process of tibial fracture after traumatic brain injury and to explore the mechanism of Nrp-1 in the formation of pathological callus after nerve injury.
 Methods: A total of 192 Wister female rats, 8-10 weeks old and weighing 220-250 g, were randomly divided into a control group (Group C), a tibia fracture group (Group F), a traumatic brain injury group (Group TBI), a traumatic brain injury combined with the tibia fracture group (Group TBI+F) (n=48 in each group). Tissue samples were collected at 3, 5, 7, 14, 21 and 28 days, respectively (n=8 for each time point). The expression of Nrp-1 in callus tissues were examined by immunohistochemistry and Western blot, while the expression of Sema3A and VEGF were detected by Western blot.
 Results: Compared with the Group F , the expression of Nrp-1 in chondrocytes of bone formation area and cartilage area was higher in the Group TBI+F, particularly at the 7th , 14th and 21st day (P<0.05), while the expression of Nrp-1 in osteoblast cells of fresh bone trabecula region was lower in the Group TBI+F, particularly at the 14th and 21st day (both P<0.05). Western blot showed that the expression of Nrp-1, Sema 3A and VEGF had the same trends in the Group TBI+F and the Group F. However, at each time point, the expression of Nrp-1 in the Group TBI+F was significantly higher and slowly decreased, particularly at the 14th, 21st and 28th day (all P<0.05). Meanwhile, the ratio of Sema 3A/VEGF in the Group TBI+F was significantly higher than that in the Group F, with statistical difference (P<0.05).
 Conclusion: The Nrp-1 is expressed abnormally in the process of fracture healing after nerve injury. It may play a role in the formation of pathological callus after nerve injury by promoting the preliminary and proliferation of chondrocytes, and inhibiting the growth of nerve fibers in the soft callus as well as the differentiation of osteoblast cell.