富血小板血浆促进面神经损伤后修复的实验研究.

Objective To investigate the protective effect and mechanism of platelet-rich plasma (PRP) on facial nerve injury. Methods A total of 100 rats were used in the experiment, in which 10 rats were used for PRP preparation, 10 rats were set as the control group (group A), and the other 80 rats were used to construct the crush model of facial nerve injury. After the surgery, the 80 rats were randomly divided into 2 groups with 40 rats in each. Group B was given continuous injection of normal saline for 1 week, which was the natural recovery group; group C was given continuous injection of PRP in the local operative area for 1 week, which was the PRP treatment group. The facial nerve function of the rats in each group was observed immediately, 1 week, 2 weeks and 3 weeks after PRP or saline intervention by behavioral and neuroelectrophysiological observation. The facial nerve was observed by electron microscopy and the glial cells were observed by hematoxylin-eosin (HE) staining. The platelet-activating growth factor (PAF), nuclear factor-κB (NF-κB) and tumor necrosis factor-α (TNF-α), brain-derived neurotrophic factor (BDNF), neurotrophic factor -4 (NT-4) in the facial nerve nucleus were detected by polymerase chain reaction (PCR). Results Behavioral evaluation: on the first day after intervention, the injury sides of group B and group C presented complete facial paralysis. Three weeks after intervention, the facial paralysis score of group C was significantly higher than that of group B, and the difference was statistically significant (P< 0.05). Neuroelectrophysiological assessment: compared with group A, the latency of facial nerve complex muscle action potentials (CMAPs) in groups B and groups C was significantly prolonged and the amplitude of CMAPs was decreased on day 1 after intervention. Three weeks after intervention, the incubation period of group C was significantly shortened and the amplitude of the wave was significantly increased. More Schwann nuclei and regenerated myelin sheath were observed in group C facial nerves under electron microscope. The facial nerve nucleus mass staining showed that the normal facial nerve motor neuron cell body was a typical multipolar motor neuron, distributed around with the glial cells. The mRNA levels of PAF, NF-κB, TNF-α, BDNF and NT-4 were all increased after injury, and the differences were all statistically significant (P <0.01). PRP reduced mRNA levels of these factors. Conclusions PRP has a protective effect on traumatic facial nerve injury, and the possible mechanisms include inhibiting the activation of PAF and the production of inflammatory mediators and upregating neurotrophic factors. [ABSTRACT FROM AUTHOR]