摘要
SUMMARY: Peripheral nerve injury is an extremely important medical and socio-economic problem. It is far from a solution, despite on rapid development of technologies. To study the effect of long-term electrical stimulation of peripheral nerves, we used a domestically produced electrical stimulation system, which is approved for clinical use. The study was performed on 28 rabbits. Control of regeneration was carried out after 3 month with morphologic techniques. The use of long-term electrostimulation technology leads to an improvement in the results of the recovery of the nerve trunk after an injury, both directly at the site of damage, when stimulation begins in the early period, and indirectly, after the nerve fibers reach the effector muscle.
La lesión de los nervios periféricos es un problema médico y socioeconómico extremadamente importante. Sin embargo, y a pesar del rápido desarrollo de las tecnologías, aún no tiene solución. Para estudiar el efecto de la estimulación eléctrica a largo plazo de los nervios periféricos, utilizamos un sistema de estimulación eléctrica de producción nacional, que está aprobado para uso clínico. El estudio se realizó en 28 conejos. El control de la regeneración se realizó a los 3 meses con técnicas morfológicas. El uso de tecnología de electro estimulación a largo plazo conduce a una mejora en los resultados de la recuperación del tronco nervioso después de una lesión, tanto directamente en el lugar del daño, cuando la estimulación comienza en el período temprano, como indirectamente, después de que las fibras nerviosas alcanzan el músculo efector.
Subject(s)
Animals , Rabbits , Electric Stimulation/methods , Peripheral Nerve Injuries/therapy , Peripheral Nerves , Muscle, Skeletal/innervation , Recovery of Function , Nerve Regeneration摘要
As the important components of peripheral nerve tissue, Schwann cells and macrophages interact with each other throughout the whole process of nerve regeneration. They play a key role in Wallerian degeneration, myelin clearance, axonal regeneration and target organ reinnervation in promotion of the repair of a peripheral nerve. In order to improve the simple strategy in treatment of peripheral nerve injury (PNI), great attention about the significance interaction mechanism between Schwann cells and macrophages in the process of nerve regeneration should be paid, as well as the continuous improvement in researches on the repair mechanism of a PNI. Trauma Centre, Shanghai General Hospital, Shanghai Jiaotong University School of Medicine summarises the interaction mechanism of Schwann cells and macrophages in the regeneration of PNI through literature reviews, from 2015 to 2023, on the mechanisms of Schwann cells and macrophages in PNI repair, hence to draw new ideas in the research and clinical treatment of PNI.
摘要
BACKGROUND:Platelet-rich plasma has been shown to enhance the viability and the pro-angiogenesis capacity of mesenchymal stem cells.Extracellular vesicles are one of the key mediators for mesenchymal stem cells to exert their effects,but currently,it is unclear whether platelet-rich plasma affects the functions of extracellular vesicles. OBJECTIVE:To investigate the effects of platelet-rich plasma on the function of extracellular vesicles from bone marrow mesenchymal stem cells,verify whether platelet-rich plasma can be used as an adjuvant to enhance the healing effects of bone marrow mesenchymal stem cells on repairing the peripheral nerve injury. METHODS:For in vitro study,bone marrow mesenchymal stem cells were cultured under normal conditions and with 1%platelet-rich plasma.The ultracentrifugation was used to extract the extracellular vesicles produced by bone marrow mesenchymal stem cells cultured under normal conditions(EVs-nor)or the condition supplemented with 1%platelet-rich plasma(EVs-prp).Extracellular vesicles were used to incubate with Schwann cells.The EdU assay,western blot assay,qPCR and light microscopy photography were performed to examine the effects of EVs-nor and EVs-prp on Schwann cell reprogramming,which was characterized by cell proliferation,c-Jun expression,reprogramming-associated gene expression and cell morphology.For in vivo study,the model of sciatic nerve injury in rats was established.Bone marrow mesenchymal stem cells were grafted with or without 1%platelet-rich plasma into the injured rat sciatic nerve using a chitin nerve conduit.Eight weeks after the surgery,the recovery was assessed by histological and functional indexes,including regenerated nerve fiber density,gastrocnemius wet weight ratio and sciatic function index. RESULTS AND CONCLUSION:(1)Compared with EVs-nor,EVs-prp was stronger in promoting Schwann cell proliferation.The gene expressions of c-Jun and GDNF were significantly upregulated in EVs-prp treated Schwann cells.The morphology of Schwann cells was significantly longer in EVs-prp group than that in EVs-nor group,indicating that EVs-prp had a stronger ability to stimulate Schwann cell reprogramming than EVs-nor.(2)Sciatic nerve injury animal experiment results revealed that grafting mesenchymal stem cells along with platelet-rich plasma into the injured sciatic nerve showed the best recovery compared with grafting mesenchymal stem cells or platelet-rich plasma alone,demonstrated by the significantly improved density of nerve fibers,gastrocnemius wet weight ratio,and sciatic function index.(3)These results suggested that platelet-rich plasma improved the function of bone marrow mesenchymal stem cell-derived extracellular vesicles and could be served as a practical and feasible preparation to synergize with bone marrow mesenchymal stem cells to improve peripheral nerve repair.
摘要
BACKGROUND:Although nerve conduits provide an effective treatment approach for nerve repair,traditional nerve conduits merely serve as mechanical channels in the repair process.The therapeutic effect still needs to be improved.Carbon nanomaterials have good physicochemical properties and hold great potential in fields such as electrochemistry and tissue engineering.Nerve conduits loaded with carbon nanomaterials,after appropriate functional modifications,are expected to further enhance the quality of nerve repair. OBJECTIVE:To review the recent research progress of carbon nanomaterial-loaded nerve conduits/scaffolds for peripheral nerve repair. METHODS:PubMed,Web of Science,China National Knowledge Infrastructure(CNKI),and Wanfang databases were searched for the literature on the application of carbon nanomaterial catheters in peripheral nerve regeneration.English keywords were"carbon nanomaterials,carbon-based nanomaterials,nerve conduit,nerve guidance conduit,scaffold,nerve regeneration,peripheral nerve repair,peripheral nerve injury"and Chinese keywords were"carbon nanomaterials,carbon materials,graphene,carbon nanotubes,nerve conduits,nerve scaffolds,nerve repair,nerve regeneration,peripheral nerve injury".Finally,69 articles were selected for this review. RESULTS AND CONCLUSION:(1)Carbon nanomaterials primarily restore damaged neural bioelectric signal conduction by activating calcium ion channels and inducing intracellular calcium activity.The application of various nerve conduit design strategies has improved the effectiveness of nerve repair.(2)Successful intraneural vascularization is the prerequisite for repairing peripheral nerve injuries.Reactive oxygen species and reactive nitrogen species generated by carbon nanomaterials trigger subsequent signaling pathways that promote intraneural vascularization.(3)The ratio of M1 to M2 macrophages affects the repair of peripheral nerve injuries.Carbon nanomaterials promote the polarization of macrophages into the M2 phenotype,thereby exerting their anti-inflammatory and regenerative effects.(4)Some carbon nanomaterials may induce excessive generation of reactive oxygen species intracellularly,potentially exhibiting cytotoxicity detrimental to nerve repair.However,appropriate functional modifications can improve the adverse effects caused by carbon nanomaterials.(5)Although carbon nanomaterials can restore the microenvironment of peripheral nerve injuries and play a positive role in promoting peripheral nerve regeneration,their inherent cytotoxicity and unclear in vivo degradation pathways still pose challenges for clinical application.However,by employing methods such as functional modification,it is possible to enhance the biocompatibility of carbon nanomaterials.Modified carbon nanomaterials have promising prospects in the field of neural tissue engineering.
摘要
A major impedance to neuronal regeneration after peripheral nerve injury(PNI)is the activation of various programmed cell death mechanisms in the dorsal root ganglion.Ferroptosis is a form of pro-grammed cell death distinguished by imbalance in iron and thiol metabolism,leading to lethal lipid peroxidation.However,the molecular mechanisms of ferroptosis in the context of PNI and nerve regeneration remain unclear.Ferroportin(Fpn),the only known mammalian nonheme iron export protein,plays a pivotal part in inhibiting ferroptosis by maintaining intracellular iron homeostasis.Here,we explored in vitro and in vivo the involvement of Fpn in neuronal ferroptosis.We first delineated that reactive oxygen species at the injury site induces neuronal ferroptosis by increasing intracellular iron via accelerated UBA52-driven ubiquitination and degradation of Fpn,and stimulation of lipid peroxidation.Early administration of the potent arterial vasodilator,hydralazine(HYD),decreases the ubiquitination of Fpn after PNI by binding to UBA52,leading to suppression of neuronal cell death and significant ac-celeration of axon regeneration and motor function recovery.HYD targeting of ferroptosis is a promising strategy for clinical management of PNI.
摘要
Artificial nerve guidance conduits (NGCs) are synthetic nerve grafts that are capable of providing the structural and nutritional support for nerve regeneration. The ideal NGCs have plenty of requirements on biocompatibility, mechanical strength, topological structure, and conductivity. Therefore, it is necessary to continuously improve the design of NGCs and establish a better therapeutic strategy for peripheral nerve injury in order to meet clinical needs. Although current NGCs have made certain process in the treatment of peripheral nerve injury, their nerve regeneration and functional outcomes on repairing long-distance nerve injury remain unsatisfactory. Herein, we review the nerve conduit design from four aspects, namely raw material selection, structural design, therapeutic factor loading and self-powered component integration. Moreover, we summarize the research progress of NGCs in the treatment of peripheral nerve injury, in order to facilitate the iterative updating and clinical transformation of NGCs.
Subject(s)
Humans , Peripheral Nerve Injuries/therapy , Guided Tissue Regeneration , Nerve Regeneration/physiology , Sciatic Nerve摘要
OBJECTIVE@#To investigate the effect of folic acid coated-crosslinked urethane-doped polyester elastomer (fCUPE) nerve conduit in repairing long distance peripheral nerve injury.@*METHODS@#Thirty-six 3-month-old male Sprague Dawley rats weighing 180-220 g were randomly assigned to 3 groups, each consisting of 12 rats: CUPE nerve conduit transplantation group (group A), fCUPE nerve conduit transplantation group (group B), and autologous nerve transplantation group (group C), the contralateral healthy limb of group C served as the control group (group D). A 20-mm-long sciatic nerve defect model was established in rats, and corresponding materials were used to repair the nerve defect according to the group. The sciatic function index (SFI) of groups A-C was calculated using the Bain formula at 1, 2, and 3 months after operation. The nerve conduction velocity (NCV) of the affected side in groups A-D was assessed using neuroelectrophysiological techniques. At 3 months after operation, the regenerated nerve tissue was collected from groups A-C for S-100 immunohistochemical staining and Schwann cell count in groups A and B to compare the level of nerve repair and regeneration in each group.@*RESULTS@#At 3 months after operation, the nerve conduits in all groups partially degraded. There was no significant adhesion between the nerve and the conduit and the surrounding tissues, the conduit was well connected with the distal and proximal nerves, and the nerve-like tissues in the conduit could be observed when the nerve conduit stents were cut off. SFI in group A was significantly higher than that in group C at each time point after operation and was significantly higher than that in group B at 2 and 3 months after operation ( P<0.05). There was no significant difference in SFI between groups B and C at each time point after operation ( P>0.05). NCV in group A was significantly slower than that in the other 3 groups at each time point after operation ( P<0.05). The NCV of groups B and C were slower than that of group D, but the difference was significant only at 1 month after operation ( P<0.05). There was no significant difference between groups B and C at each time point after operation ( P>0.05). Immunohistochemical staining showed that the nerve tissue of group A had an abnormal cavo-like structure, light tissue staining, and many non-Schwann cells. In group B, a large quantity of normal neural structures was observed, the staining was deeper than that in group A, and the distribution of dedifferentiated Schwann cells was obvious. In group C, the nerve bundles were arranged neatly, and the tissue staining was the deepest. The number of Schwann cells in group B was (727.50±57.60) cells/mm 2, which was significantly more than that in group A [(298.33±153.12) cells/mm 2] ( t=6.139, P<0.001).@*CONCLUSION@#The fCUPE nerve conduit is effective in repairing long-distance sciatic nerve defects and is comparable to autologous nerve grafts. It has the potential to be used as a substitute material for peripheral nerve defect transplantation.
Subject(s)
Rats , Animals , Male , Rats, Sprague-Dawley , Polyesters , Peripheral Nerve Injuries/surgery , Elastomers , Urethane , Sciatic Nerve/injuries , Carbamates , Nerve Tissue , Nerve Regeneration/physiology摘要
The recovery of motor and sensory functions after peripheral nerve injury has been an important concern in the medical field, and axonal regeneration and re-innervation of the corresponding target organs is important prerequisites for recovery of motor and sensory functions. Cyclic adenosine monophosphate (cAMP) is an intracellular second messenger that affects the damage repair in human tissues. Protein kinase A (PKA) and exchange protein activated by cAMP (EPAC), downstream factors of cAMP, are closely related to nerve regeneration, and they are involved in and play a key role in axonal regeneration. In this paper, we review the effect of cAMP signaling pathway on myelin debris removal, axon guidance, and growth cone regeneration after peripheral nerve injury.
摘要
Recent studies have shown that Schwann cells (SCs) can effectively promote peripheral nerve regeneration under physical modulation of mechanical retraction, electricity, magnetism, light, and extracorporeal shock waves, whose neural signaling pathways involve Janus kinase/signal transduction and transcriptional activator (JAK-STAT) pathway, mitogen-activated protein kinase (MAPK) pathway, Notch pathway, and neuregulin 1 (NRG1) pathway. In this paper, we summarize the role and mechanism of SCs in peripheral nerve regeneration, as well as the therapeutic strategies based on SCs to promote peripheral nerve repair in recent years, aiming to provide references for clinical treatment of peripheral neuropathy.
摘要
OBJECTIVE To explore the mechanism of Taohong siwu decoction （THD） improving peripheral nerve injury induced by paclitaxel （PTX） in rats. METHODS The effects of THD （1 g/mL drug-containing serum） and PTX （0.1 μmol/L） alone or in combination on the proliferation rate of Schwann cells line RSC96 as well as the expressions of lysosomal-associated membrane protein-2 （LAMP2）， autophagy marker protein yeast Atg 6 homolog （Beclin1）， phosphatidylinositol 3-kinase （PI3K）， protein kinase B （Akt）， and mammalian target of rapamycin （mTOR） were investigated， and then compared with autophagy promoter rapamycin and autophagy inhibitor 3-methyladenine （3-MA）. The effects of high-dose and low-dose THD on the expressions of myelin basic protein （MBP） and myelin protein zero （MPZ）， S100 calcium-binding protein （S100）， LAMP2， Beclin1， PI3K， Akt and mTOR were tested at the end of the experiment. RESULTS After treatment of THD+PTX， the proliferation rate of RSC96 cells was significantly higher than those treated with PTX alone. After treatment of THD+PTX or THD+ 3-MA， the protein expressions of LAMP2 and Beclin1 in RSC96 cells were significantly higher than those treated with PTX or 3- MA alone， while the protein expressions of PI3K， Akt and mTOR were significantly lower than those treated with PTX or 3-MA alone （P＜0.05）. Compared with model group， the protein expressions of MBP， MPZ， S100， LAMP2 and Beclin1 in sciatic nerve of rats were increased significantly in THD high-dose and low-dose groups， while the protein expressions of PI3K， Akt and mTOR were significantly decreased （P＜0.05）. CONCLUSIONS THD may activate Schwann cell autophagy by inhibiting the PI3K/Akt/ mTOR signaling pathway， thereby improving peripheral nerve injury caused by PTX.
摘要
Objective: To analyze clinical features and electroneuromyography (ENMG) results of chronic mild occupational carbon disulfide poisoning cases. Methods: A total of 344 patients diagnosed with chronic mild occupational carbon disulfide poisoning based on GBZ 4-2002 Diagnostic Criteria of Occupational Chronic Carbon Disulfide Poisoning were selected as study subjects from 2006 to 2019 using the retrospective study method. Their clinical data was collected and analyzed. Results: The main symptoms of the study subjects were dizziness, headache, insomnia, dreaming, memory impairment, numbness and weakness in the distal extremities. Positive signs mainly included symmetrical glove and stocking distribution like sensory disorders in the distal extremities, and the weakening or absent Achilles tendon reflex and knee reflex. The incidence of symptoms and signs increased with the length of service (all P<0.01). The incidence of fundus and venous changes in patients was 41.3%, which increased with the length of service (P<0.01). ENMG examination showed varying degrees of abnormalities in the peripheral motor and/or sensory nerves in all patients, with a higher incidence of motor nerve abnormalities than sensory nerve abnormalities (21.1% vs 3.7%, P<0.01). The incidence of motor nerve abnormality was higher on the right side than the left side (23.7% vs 18.5%, P<0.01). The incidences of motor nerve abnormalities from high to low in the order were median nerve, common peroneal nerve, ulnar nerve and posterior tibial nerve (34.9% vs 27.9% vs 16.6% vs 5.1%, P<0.01). The incidences of sensory nerve abnormalities from high to low in the order were median nerve, ulnar nerve and sural nerve (5.2% vs 5.1% vs 0.7%, P<0.01). The incidences of left ulnar nerve, right ulnar nerve and right median nerve were higher in male patients than in female patients (15.2% vs 5.3%, 24.0% vs 11.7%, 44.8% vs 28.7%, all P<0.05), while the incidences of the left and right common peroneal nerve in lower extremity motor nerve were lower in male patients than in female patients (18.4% vs 52.1%, 21.2% vs 46.8%, all P<0.01). Conclusion: Chronic mild occupational carbon disulfide poisoning was mainly manifested as multiple peripheral nerve injury. ENMG results showed that the distal motor nerve conduction abnormalities were more sensitive than the sensory nerve conduction abnormalities, with a higher degree of impairment in the upper limb than the lower limb, and more impairment in the right side than the left side.
摘要
Oxidative stress plays a role in the delay of peripheral nerve regeneration after injury. The accumulation of free radicals results in nerve tissue damage and dorsal root ganglion (DRG) neuronal death. Pinostrobin (PB) is one of the bioflavonoids from Boesenbergia rotunda and has been reported to possess antioxidant capacity and numerous pharmacological activities. Therefore, this study aimed to investigate the effects of PB on peripheral nerve regeneration after injury. Male Wistar rats were randomly divided into 5 groups including control, sham, sciatic nerve crush injury (SNC), SNC + 20 mg/kg PB, and SNC + 40 mg/kg PB. Nerve functional recovery was observed every 7 days. At the end of the study, the sciatic nerve and the DRG were collected for histological and biochemical analyses. PB treatment at doses of 20 and 40 mg/kg reduced oxidative stress by up-regulating endogenous glutathione. The reduced oxidative stress in PB-treated rats resulted in increased axon diameters, greater number of DRG neurons, and p-ERK1/2 expression in addition to faster functional recovery within 4 weeks compared to untreated SNC rats. The results indicated that PB diminished the oxidative stress-induced nerve injury. These effects should be considered in the treatment of peripheral nerve injury.
摘要
Introdução: As lesões nervosas periféricas (LNP) podem resultar em distúrbios motores e sensoriais alterando a funcionalidade do membro afetado, porém pouco se conhece a respeito dos efeitos da fotobiomodulação (FBM) com diodo emissor de luz (LED). Objetivo: Analisar os efeitos do LED sobre a funcionalidade da marcha de ratos Wistar pós LNP. Metodologia: Ratos Wistar foram submetidos a LNP por esmagamento de ciático e analisados nos seguintes grupos experimentais: (1) Controle; (2) LNP; (3) LNP+ LED (780 nm, potência média 40 mW, exposição radiante, energia por ponto, 3,2 J sobre o nervo ciático (LEDn); (4) LNP+ LED em nervo e região do músculo envolvido (LEDnm) e (5) LNP+ LED apenas em região do músculo (LEDm). Após 7, 14, 21 e 28 dias foram realizadas as análises de marcha utilizando o Índice Funcional Ciático (IFC). Resultado: Após 7 dias, os grupos tratados com LED apresentaram uma melhora da marcha em relação ao grupo Lesão, sendo essa melhora mais pronunciada no grupo LEDn. Após 14 dias, os grupos LEDn e LEDnm apresentaram valores semelhantes ao grupo controle e após 21 e 28 dias o IFC não apresentou diferenças entre os grupos experimentais. Conclusão: O LED aumentou a funcionalidade da marcha avaliada pelo IFC após 1 e 2 semanas pós LNP, especialmente quando foi usado na região nervosa associada ou não à região muscular.
Introduction: Peripheral nerve injuries (PNI) can result in motor and sensory disturbances altering the functionality of the affected limb, however not much is known about the effects of photobiomodulation (PBM) with light emitting diode (LED). Objective: We aimed to analyze the effects of LED on the gait function of Wistar rats after PNI. Methodology: Wistar rats were submitted to PNI by sciatic crush and analyzed in the following experimental groups: (1) Control; (2) PNI; (3) PNI+ LED (780 nm, mean power 40 mW, radiant exposure, energy per spot, 3.2 J on the sciatic nerve) (LEDn); (4) LNP+ LED on nerve and involved muscle region (LEDnm) and (5) LNP+ LED only on muscle region (LEDm). After 7-, 14-, 21- and 28-days gait analyses were performed using the Sciatic Functional Index (SFI). Results: After 7 days, the groups treated with LED showed an improvement in gait compared to the PNI group, with this improvement being more pronounced in the LEDn group. After 14 days, the LEDn and LEDnm groups showed similar values to the control group and after 21 and 28 days the SFI did not show differences between the experimental groups. Conclusion: LED increased the gait functionality evaluated by SFI after 1 and 2 weeks post-PNI, especially when it was used in the nerve region associated or not with the muscle region.
摘要
Aim To investigate the role of collybistin in the regulation of pain transmission. Methods The distribution of collybistin in spinal cord was observed by immunohistochemical staining. The role of collybis¬tin in pain transmission was evaluated by behavioral experiments. The effect of collybistin on inhibitory synap¬tic transmission was studied by electrophysiological ex¬periments. Results Collybistin was distributed in spi¬nal cord neurons; ShRNA-collybistin induced pain sen-sitization of intact mice ( P < 0. 05 ) . Overexpression of collybistin in spinal cord significantly alleviated pain sensitization induced by peripheral nerve injury ( P <0. 05 ) . ShRNA-collybistin also significantly reduced the amplitudes and frequencies of miniature inhibitory postsynaptic currents (mlPSCs) in superficial neurons of spinal cord dorsal horn (P <0. 05) . Overexpression of collybistin in spinal cord could reverse the effects of peripheral nerve injury on mlPSCs (P <0. 05). Con¬clusions Collybistin is involved in pain sensitization induced by peripheral nerve injury in mice.
摘要
Enhancing remyelination after injury is of utmost importance for optimizing the recovery of nerve function. While the formation of myelin by Schwann cells (SCs) is critical for the function of the peripheral nervous system, the temporal dynamics and regulatory mechanisms that control the progress of the SC lineage through myelination require further elucidation. Here, using in vitro co-culture models, gene expression profiling of laser capture-microdissected SCs at various stages of myelination, and multilevel bioinformatic analysis, we demonstrated that SCs exhibit three distinct transcriptional characteristics during myelination: the immature, promyelinating, and myelinating states. We showed that suppressor interacting 3a (Sin3A) and 16 other transcription factors and chromatin regulators play important roles in the progress of myelination. Sin3A knockdown in the sciatic nerve or specifically in SCs reduced or delayed the myelination of regenerating axons in a rat crushed sciatic nerve model, while overexpression of Sin3A greatly promoted the remyelination of axons. Further, in vitro experiments revealed that Sin3A silencing inhibited SC migration and differentiation at the promyelination stage and promoted SC proliferation at the immature stage. In addition, SC differentiation and maturation may be regulated by the Sin3A/histone deacetylase2 (HDAC2) complex functionally cooperating with Sox10, as demonstrated by rescue assays. Together, these results complement the recent genome and proteome analyses of SCs during peripheral nerve myelin formation. The results also reveal a key role of Sin3A-dependent chromatin organization in promoting myelinogenic programs and SC differentiation to control peripheral myelination and repair. These findings may inform new treatments for enhancing remyelination and nerve regeneration.
Subject(s)
Animals , Rats , Axons , Chromatin/metabolism , Gene Expression Profiling , Myelin Sheath/metabolism , Nerve Regeneration/physiology , Schwann Cells/metabolism , Sciatic Nerve/injuries摘要
This article reviews the research progress in promotion of peripheral nerve regeneration by regulating macrophages, a new idea for the research and treatment of peripheral nerve injury. The Trauma Center of The First People's Hospital Affiliated to Shanghai Jiao Tong University reviewed the relevant literatures in the regulation of macrophages on peripheral nerve regeneration at home and abroad, from 2013 to 2021, were reviewed and analysed. Of the study from 2013 to 2021, autologous nerve transfer was the main option in the treatment of peripheral nerve injury, but it has many setbacks such as insufficient donor, new nerve injury and local neuroma. Modulating macrophage-related function can effectively improve the prognosis of nerve injury. In recent years, the regulation of macrophages in the treatment of nerve injury is mainly through the mechanism of M1 macrophages polarisation to M2 macrophages, increase of phagocytosis, change of the phenotype of macrophages, and so on. By studying the characteristics of macrophages and regulating the function and phenotype of macrophages, it would provide a new idea and important research direction in the treatment of peripheral nerve injury.
摘要
@#Abstract: Methods - （ ） To investigate the repairing effect of adipose derived stem cells ADSCs transplantation in - - Methods 1 bromopropane induced peripheral nerve injury in rats. A total of 45 specific pathogen free male SD rats were （ ） （ ） randomly assigned to the control group 15 rats and exposure group 30 rats . The rats in the exposure group were gavaged with - ， ， 1 bromopropane at a dose of 800 mg/kg body weight while the control group were given with equal volume of corn oil once a ， - day five days per week for eight weeks. The rat model of peripheral nerve injury induced by 1 bromopropane was established - ， - and was randomly assigned to the self recovery group and ADSCs group 12 rats in each group. ADSCs group and self recovery （ 6 ） ， group were injected with 0.5 mL contains 1×10 cells ADSCs or 0.5 mL phosphate buffer solution respectively by tail vein once a week for four weeks. The control group was not administered any treatment. The rats in each group were assessed using - - （ ） ， ， inclined plane test and Basso Beattie Bresnahan BBB score on the first day before treatment as well as 7 14 21 and 28 day ， after treatment. At the end of treatment the sciatic nerve was isolated for histopathological examination. The oxidative stress - indexes in the cerebral motor cortex were detected by colorimetric analysis. The levels of brain derived neurotrophic factor （ ） （ ） - Results BDNF and nerve growth factor NGF in the sciatic nerve were detected by enzyme linked immunosorbent assay. The - maximum tilt angle of the inclined plate and the BBB score were lower in self recovery group at the five time points of treatment （ P< ） all 0.05 compared with the control group. The maximum tilt angle of the inclined plate test was higher in ADSCs group at 21 （ P< ）， ， ， （ P< ）， and 28 days of treatment all 0.05 and the BBB score was higher at 7 14 21 and 28 days of treatment all 0.05 - （ ） when compared with the self recovery group. The level of malondialdehyde MDA in the cerebral motor cortex increased （P< ）， （ ） （ ） （ P< ）， 0.05 while the superoxide dismutase SOD activity and glutathione GSH level decreased all 0.05 and the levels （ P< ） - of BDNF and NGF in the sciatic nerve decreased all 0.05 in self recovery group compared with the control group. There was ， ， no significant difference in SOD activity and MDA GSH BDNF and NGF levels between ADSCs group and control group （ P> ） （P< ）， （ all 0.05 . The level of MDA in cerebral motor cortex decreased 0.05 the SOD activity and GSH level increased all P< ）， （P< ） - 0.05 and the level of BDNF in sciatic nerve increased 0.05 in ADSCs group compared with the self recovery group. Conclusion - - ADSCs transplantation can repair peripheral nerve injury induced by 1 bromopropane via anti oxidative stress and regulating the secretion of neurotrophic factors.
摘要
Due to the limited self-repair ability of neurons after injury, there has been a lack of effective treatments for nerve injury in clinical practice. So, to find drugs that promote the repair after nerve injury has become a research hotspot. Schwann cells and neurons play an important role in regeneration of the peripheral nerves after injury. This review summarizes the classification of peripheral nerve injury, the signaling pathways related to peripheral nerve regeneration in Schwann cells and neurons as well as diseases related to peripheral nerve injury, and provides a basis for further exploration of the regeneration mechanism after peripheral nerve injury.
摘要
@#Peripheral nerve injury (PNI) is a common disease in the oral cavity that can easily lead to loss of function and abnormal appearance. The application of dental pulp stem cells (DPSCs) combined with tissue engineering in the repair of PNI is a research hotspot. DPSCs have the advantages of abundant sources, simple extraction, low immunogenicity and a high proliferation rate in vitro. They can differentiate into Schwann cells (SCs). SCs can induce autophagy and secrete key neurotrophic factors, such as nerve growth factor, brain-derived neurotrophic factor, ciliary neurotrophic factor and glial cell-derived neurotrophic factor. SCs are beneficial for the repair of nerve injury. DPSCs in different periods have differences in immune regulation, anti-inflammatory effects, expression of neural markers, angiogenesis and so on, which provide more diversified choices for nerve repair. At present, the introduction of tissue engineering provides a more controllable and improved microenvironment for DPSCs, which is conducive to the application and development of DPSCs in regenerative medicine and tissue engineering. However, there are still many problems to be solved, such as the selection of stem cells, functional link recovery, uncontrollable direction of axon regeneration, regulation of the peripheral nervous system and mechanism of repair.
摘要
BACKGROUND: Non-coding RNA is widely distributed in the nervous system in vivo and a significant change in the expression of non-coding RNA has been observed in a neural injury model. This suggests that non-coding RNA may serve as a potential target for resolving the challenges of peripheral nerve repair. OBJECTIVE: To summarize the mechanisms of microRNA, circular RNA and long non-coding RNA in the process of repair after peripheral nerve injury with the attempt to determine the possible treatment of peripheral nerve injury. METHODS: The first author retrieved the relevant literatures in CNKI and PubMed databases published from January 2001 to April 2019. The key words were “non-coding RNA, miRNA, circRNA, IncRNA, peripheral nerve injury” in Chinese and English, respectively. Forty-three literatures were included in accordance with the exclusion and inclusion criteria. RESULTS AND CONCLUSION: (1) MicroRNAs can act on certain signal pathways, regulate the apoptosis, growth, proliferation and differentiation of Schwann cells and participate in the repair of peripheral nerve injury. (2) Circular RNAs act as microRNA sponges to competitively inhibit the transcription in microRNA, and exert corresponding biological functions. (3) A large amount of long non-coding RNAs are expressed after peripheral nerve injury, and play a key role in the peripheral nerve regeneration.