Objective To investigate the therapeutic effects of nano-hydroxyapatite/polyamide 66/platelet-rich plasma com-pound(n-HA/PA66/PRP)on the recovery of rabbit femur bone defect.Methods 40 New Zealand rabbits were artificially made to be bone defect by resecting the 1 cm substantia ossea with periosteum of femur,and were divided into two groups averagely depen-ding on implanted materials:experimental group(n-HA/PA66/PRP),control group (n-HA/PA66).Every five rabbits were sacri-ficed on week 2,4,8,12,and the femur healing status was observed by X ray,histology,and immunohistochemistry.Results No rabbit was infected or died,no implantation objects dropped.Gross observation,X-ray result and histology results demonstrated that the experimental group began to have a new bone tissue at 2 weeks after the operation,with the extension of time,the experimental group new bone growth speed and the quantity was better than the control group.The Lane-Sandhu method X-ray score showed that the experimental group (6.80±2.05)points and the control group(4.20±1.30)points at 12 weeks after the operation,and there were significant differences between two groups(P <0.05).Immunohistochemistry indicated that expression intensity of Vas-cular endothelial growth factor at 2 weeks and 4 weeks were significant differences between two groups(P <0.05),but there was no significant difference at 8 weeks and 12 weeks (P >0.05).Conclusion PRP combined with n-HA/PA66 artificial bone could accel-erate the healing of bone defect,and the effect of repair of bone defect is better than that of n-HA/PA66 artificial bone in the early.

BACKGROUND:After spinal cord injury, endogenous neural stem cel s are activated to proliferate and migrate to repair damaged tissue. As a clinical medicine, methylprednisolone shows a lot of functions, but its effects on endogenous neural stem cel s are stil unknown.
OBJECTIVE:To explore the effects of methylprednisolone on the proliferation and migration of endogenous neural stem cel s after spinal cord injury.
METHODS:Seventy-five Sprague-Dawley rats were used to make animal models of T10 complete paraplegia using Al en’s method, and randomized into methylprednisolone, normal saline and model groups. Rats in these three groups were given intraperitoneal injection of 1 g/L methylprednisolone solution at a dose of 30 mg/kg for 10 minutes and at a dose of 5.4 mg/kg/h for 23 hours, given intraperitoneal injection of normal saline at the same dose and given no treatment, respectively. Neurological and motor functions were assessed by somatosensory evoked potential and Basso Beattie Bresnahan scores at 7, 14, 21, 28 days after spinal cord injury. BrdU and Nestin staining of the injured spinal cord segment was conducted.
RESULTS AND CONCLUSION:A large amount of BrdU-and Nestin-positive cel s were visible in al the groups, and the number of these cel s reached the peach at 14 days after spinal cord injury. Methylprednisolone was found to inhibit BrdU-, Nestin-or double-positive cel s, indicating methylprednisolone can inhibit the proliferation and migration of endogenous neural stem cel s. The results of Basso Beattie Bresnahan scores showed no notable improvement in the motor function of the limbs. Methylprednisolone also showed no significant effects on the motor evoked potential latency, but promoted nerve conduction recovery. Al these findings indicate that methylprednisolone has some hindering effects on spinal cord repair by inhibiting the proliferation and migration of endogenous neural stem cel s after spinal cord injury.