OBJECTIVE Following the delayed repair of peripheral nerve injury, the cell number of anterior horn of the spinal cord and its ultrastructural changes, motorneuron and its electrophysiological changes were investigated. METHODS In 16 rabbits the common peroneal nerves of both sides being transected one year later were divided into four groups randomly: the degeneration group and regeneration of 1, 3 and 5 months groups. Another 4 rabbits were used for control. All transected common peroneal nerves underwent epineural suture except for the degeneration group the electrophysiological examination was carried out at 1, 3 and 5 months postoperatively. Retrograde labelling of the anterior horn cells was demonstrated and the cells were observed under light and electronmicroscope. RESULTS 1. The number of labelled anterior horn cell in the spinal cord was 45% of the normal population after denervation for one year (P lt; 0.01). The number of labelled cells increased steadily from 48% to 57% and 68% of normal values at 1, 3 and 5 months following delayed nerve repair (P lt; 0.01). 2. The ultrastructure of the anterior horn cells of the recover gradually after repair. 3. With the progress of regeneration the latency become shortened, the conduction velocity was increased, the amplitude of action potential was increased. CONCLUSION Following delayed repair of injury of peripheral nerve, the morphology of anterior horn cells of spinal cord and electrophysiological display all revealed evidence of regeneration, thus the late repair of injury of peripheral nerve was valid.
To observe the change of morphology and neuropeptide in the spinal neurons in order to clarify the functional state after injury of peripheral nerves is especially in the late stage. Sciatic nerves were cut with their proximal segments in the preparation of a model of peripheral nerve injury. Combination of horseradish peroxidase retrograde tracing immunohistochemistry and computer image analysis the changes in the morphometry of the perikarya of ventral horn neurons of the spinal cord, the quantitative changes of substance P (SP). Calcitonin gene-related peptide (CGRP) in dorsal horn and CGRP and choline acetyransferase (CHAT) in ventral horn of the spinal cord were examed. The results showd: (1) At the 3rd week after injury, swollen perikarya of the ventral horn neurons were observed, subseauently the swelling of perikarya was decreased tile the 6th week the neurons recovered to their normal size. At the 12th week the neurons were generally stable in their size, shortening of the dendrites was seen in 27% of the neurons. (2) The dendrites of the neurons progressively contracted till at the 12th week 53% of them were degenerated. The results of the 24th week were similar to the that at the 12th week. (3) CGRP in the ventral horn of the spinal cord was elevated to the highest point after 1 week of injury, that lasting for 4 weeks and 8 weeks later, the lever of CGRP returned to normal. From 20th to 24th week, there was no obvious changes of CHAT in the ventral horn of the spinal cord during observation. (4) SP went to the lowest point in the dorsal horn during 2-6 weeks, then recovered slowly, and beiny normal again after 16 weeks, however, CGRP was changed slightly. The results indicated that although a series of degenerating changes occurred in the neurons of the spinal cord during the late peripheral nerve injury, but the functional activity of the central meurons still was maintained at a certain level.
Objective To explore effects of several immunosuppressants on cytokine expressions after repair for a sciatic nerve injury in a rat model. Methods The sciatic nerves of 42 rats were cut and suturedend to end. After operation, the rats were divided into 6 groups. Group A(n=9) was served as a control with no medicines given. Group B (n=9) was given methylprednisolone 20 mg/(kg·d) for 2 days. Groups C(n=9) and D(n=3) were given FK506 1 mg/(kg·d) for 2 weeks and 4 weeks respectively, and were given the same doses of methylprednisolone as Group B. Groups E and F were given CsA 2 mg/(kg·d) for 2 weeks and 4 weeks respectively, and were given the same doses of methylprednisolone as Group B. The sciaticnerves were sampled at 1, 2 and 4 weeks postoperatively. And immuneohistochemistry stainings of interleukin 1β(IL-1β)， tumor necrosis factor α(TNF-α), interferon γ(IFN-γ) and macrophage migration inhibitory factor(MIF) were performed. The staining results were compared and analyzed. Results The expression peaks of IL-1β and IFN-γ were found at the 1st week postoperatively in Group A. Then, the expression decreased rapidly at the 2nd week and disappeared at the 4th week. As for TNF-α and MIF, they were only found to have a low expression until the 1st week in Group A. In groups C-F, the expression peaks of IL-1β, TNF-α and IFN-γ were found at the 2nd week, while the expression peak of MIF was still at the 1st week, and the expression of all the cytokines extended to the 4th week. The expressions of these cytokines in Group B were just between the expression levels of Group A and Groups C-F. Conclusion Immunosuppressants can delay the expression peaks and significantly extend the expression time of IL-1β, TNF-α, IFN-γ and MIF after repair for a sciatic nerve injury in a rat model.
ObjectiveTo summarize the regulatory role of long non-coding RNA (lncRNA) in peripheral nerve injury (PNI) and neural regeneration.MethodsThe characteristics and mechanisms of lncRNA were summarized and its regulatory role in PNI and neural regeneration were elaborated by referring to relevant domestic and foreign literature in recent years.ResultsNeuropathic pain and denervated muscle atrophy are common complications of PNI, affecting patients’ quality of life. Numerous lncRNAs are upregulated after PNI, which promote the progress of neuropathic pain by regulating nerve excitability and neuroinflammation. Several lncRNAs are found to promote the progress of denervated muscle atrophy. Importantly, peripheral nerve regeneration occurs after PNI. LncRNAs promote peripheral nerve regeneration through promoting neuronal axonal outgrowth and the proliferation and migration of Schwann cells.ConclusionAt present, the research on lncRNA regulating PNI and neural regeneration is still in its infancy. The specific mechanism remains to be further explored. How to achieve clinical translation of experimental results is also a major challenge for future research.
ObjectiveTo summarize the research status of mandibular sensory dysfunction after transoral endoscopic thyroidectomy vestibular approach (TOETVA), and explore its potential treatment methods and existing problems, and provide ideas and methods for future clinical treatments or research. MethodThe domestic and foreign literatures about peripheral nerve injury and its treatment after TOETVA were searched and reviewed. ResultsMental nerve injury was considered to be the main cause of mandibular sensory dysfunction after TOETVA. Due to the lack of unified definitions and assessment standards, the true incidence remained unclear. In order to reduce the risk of mental nerve injury, methods such as exposing the mental nerve and combining vestibular approaches during surgery had certain advantages. In terms of treatment, several methods promoting nerve repair were noteworthy, including B vitamins, nerve growth factors, physical therapy and so on. In addition, some auxiliary treatments of Traditional Chinese Medicine also showed effectiveness in promoting nerve regeneration. ConclusionsIt is essential to avoid damage to the mental nerve and mandibular tissues during surgery. For patients with significant complaints postoperatively, active treatment should be pursued. Establishing objective and quantifiable standards for evaluating mandibular sensory dysfunction and seeking effective clinical plans through a multidisciplinary approach may be the direction for future research.
Objective To study the effect of olfactory ensheathingcells(OECs) transplantation on protecting spinal cord and neurons after peripheral nerve injury. Methods Fifty-five SD rats were randomly divided into blank group (n=5), experimental group (n=25) and control group (n=25). The right sciatic nerves of all the rats were transected. The proximal end was embedded in muscle and treated with OECs (experimental group) and DMEM (control group). No treatment was given to the blank group. The rats were sacrificed 1, 2, 3, 7, and 14 days after the transplantation, the related neurons were observed with histological and TUNEL methods. Results After sciatic nerves were transected, death of neurons occurred in spinal cord and ganglion. One, 2, 3 days after treatment, the neuron survival rate in experimental group was 98.4％±6.5%，97.6％±6.5%，95.2％±6.7% respectively. The neuron survival rate in control group was 97.8％±6.7%，97.4％±6.4%，94.3％±6.8% 1, 2, and 3 days after treatment respectively. There was no significant difference between experimental group and control group. Seven and 14 days after treatment, the neuron survival rate in experimental group was 92.4％±8.9%，87.7％±9.4% respectively. The neuron survival rate in control group was 87.4％±8.6%，83.4％±8.5% 7 and 14 days after treatment respectively. There was significant difference between experimental group and control group. On 1st and 2nd day, no apoptosis was seen in spinal cord anterior horn of the rats in both experimental group and control group. On 3rd, 7th, and 14th day, the apoptosis index of spinal cord anterior horn motoneuron in experimental rats were lower（1.2±0.8，1.4±0.6，4.1±1.3） than that in the control group（2.1±1.1，3.1±1.1，6.1±1.8）（Plt;0.05）. One, 2, and 3 days after the operation, no ganglion neurons apoptosis was observed in all rats. On 7th day the apoptosis index of ganglion neurons in experimental group（2.10±0.32）were lower than thatin control group （4.40±0.56）（Plt;0.05）. On 14th day there was no significant difference in the apoptosis index of ganglion neurons between experimental group （4.30±1.80）and control group（6.70±2.50）(P＜0.05). Conclusion Apoptosis of neurons occur after peripheral nerve injury in spinal cord and ganglion. OECs transplantation is effective in preventing apoptosis.
Objective To review the research progress on silk fibroin (SF)-nerve guidance conduits (NGCs) for peripheral nerve injury (PNI) repair. Methods To review the recent literature on PNI and SF-NGCs, expound the concepts and treatment strategies of PNI, and summarize the construction of SF-NGCs and its application in PNI repair. Results Autologous nerve transplantation remains the “gold standard” for treating severe PNI. However, it’s clinical applications are constrained by the limitations of limited donors and donor area damage. Natural SF exhibits good biocompatibility, low immunogenicity, and excellent physicochemical properties, making it an ideal candidate for the construction of NGCs. SF-NGCs constructed using different technologies have been found to have better biocompatibility and bioactivity. Their configurations can facilitate nerve regeneration by enhancing regenerative guidance and axonal extension. Besides, the adhesion, proliferation and differentiation of neurons and Schwann cells related to PNI repair can be effectively promote by NGCs. This accelerates the speed of nerve regeneration and improves the efficiency of repair. In addition, SF-NGCs can be used as regenerative scaffolds to provide biological templates for nerve repair. Conclusion The biodegradable natural SF has been extensively studied and demonstrated promising application prospects in the field of NGCs. It might be an effective and viable alternative to the “gold standard” for PNI treatment.