Repair Of Nerve Injury Research Articles

VEGFA-modified DPSCs combined with LC-YE-PLGA NGCs promote facial nerve injury repair in rats

ObjectiveThe aim of this research was to investigate the effect of vascular endothelial growth factor A (VEGFA)-overexpressing rat dental pulp stem cells (rDPSCs) combined with laminin-coated and yarn-encapsulated poly(l-lactide-co-glycolide) (PLGA) nerve guidance conduit (LC-YE-PLGA NGC) in repairing 10 mm facial nerve injury in rats. Study DesignrDPSCs isolated from rat mandibular central incisor were cultured and identified in vitro and further transfected with the lentiviral vectors (Lv-VEGFA). To investigate the role and mechanisms of VEGFA in neurogenic differentiation in vitro, semaxanib (SU5416), Cell Counting Kit-8 (CCK-8), real-time quantitative polymerase chain reaction (qPCR) and Western blotting were performed. Ten-millimeter facial nerve defect models in rats were established and bridged by LC-YE-PLGA NGCs. The repair effects were detected by transmission electron microscopy (TEM), compound muscle action potential (CMAP), immunohistochemistry and immunofluorescence. ResultsExtracted cells exhibited spindle-shaped morphology, presented typical markers (CD44+CD90+CD34−CD45−), and presented multidirectional differentiation potential. The DPSCs with VEGFA overexpression were constructed successfully. VEGFA enhanced the proliferation and neural differentiation ability of rDPSCs, and the expression of neuron-specific enolase (NSE) and βIII-tubulin was increased. However, these trends were reversed with the addition of SU5416. This suggests that VEGFA mediates the above effects mainly through vascular endothelial growth factor receptor 2 (VEGFR2) binding. The LC-YE-NGC basically meet the requirements of facial nerve repair. For the in vivo experiment, the CMAP latency period was shorter in DPSCS-VEGFA-NGC group in comparison with other experimental groups, while the amplitude was increased. Such functional recovery correlated well with an increase in histological improvement. Further study suggested that VEGFA-modified DPSCs could increase the myelin number, thickness and axon diameter of facial nerve. NSE, βIII-tubulin and S100 fluorescence intensity and immunohistochemical staining intensity were significantly enhanced. ConclusionVEGFA-modified rDPSCs combined with LC-YE-PLGA NGCs have certain advantages in the growth and functional recovery of facial nerves in rats.

Primary Repair versus Reverse End-to-Side Coaptation by Anterior Interosseous Nerve Transfer in Proximal Ulnar Nerve Injuries.

Proximal ulnar nerve lacerations are challenging to treat because of the complex integration of sensory and motor function in the hand. The purpose of this study was to compare primary repair and primary repair plus anterior interosseous nerve (AIN) reverse end-to-side (RETS) coaptation in the setting of proximal ulnar nerve injuries. A prospective cohort study was performed of all patients at a single, academic, level I trauma center from 2014 to 2018 presenting with isolated complete ulnar nerve lacerations. Patients underwent either primary repair (PR) only or primary repair and AIN RETS (PR + RETS). Data collected included demographic information; quick Disabilities of the Arm, Shoulder and Hand questionnaire score; Medical Research Council score; grip and pinch strength; and visual analogue scale pain scores at 6 and 12 months postoperatively. Sixty patients were included in the study: 28 in the PR group and 32 in the RETS + PR group. There was no difference in demographic variables or location of injury between the two groups. Average quick Disabilities of the Arm, Shoulder and Hand questionnaire scores for the PR and PR + RETS groups were 65 ± 6 and 36 ± 4 at 6 months and 46 ± 4 and 24 ± 3 at 12 months postoperatively, respectively, and were significantly lower in the PR + RETS group at both points. Average grip and pinch strength were significantly greater for the PR + RETS group at 6 and 12 months. This study demonstrated that primary repair of proximal ulnar nerve injuries plus AIN RETS coaptation yielded superior strength and improved upper extremity function when compared with PR alone. Therapeutic, II.

Research Progress of Low-Intensity Pulsed Ultrasound in the Repair of Peripheral Nerve Injury.

Peripheral nerve injury (PNI) is a common disease that has profound impact on the health of patients, but has poor prognosis. The gold standard for the treatment of peripheral nerve defects is autologous nerve grafting; notwithstanding, due to the extremely high requirement for surgeons and medical facilities, there is great interest in developing better treatment strategies for PNI. Low-intensity pulsed ultrasound (LIPUS) is a noninterventional stimulation method characterized by low-intensity pulsed waves. It has good therapeutic effect on fractures, inflammation, soft tissue regeneration, and nerve regulation, and can participate in PNI repair from multiple perspectives. This review concentrates on the effects and mechanisms of LIPUS in the repair of PNI from the perspective of LIPUS stimulation of neural cells and stem cells, modulation of neurotrophic factors, signaling pathways, proinflammatory cytokines, and nerve-related molecules. In addition, the effects of LIPUS on nerve conduits are reviewed, as nerve conduits are expected to be a successful alternative treatment for PNI with the development of tissue engineering. Overall, the application advantages and prospects of LIPUS in the repair of PNI are highlighted by summarizing the effects of LIPUS on seed cells, neurotrophic factors, and nerve conduits for neural tissue engineering.

Hypoxic culture of umbilical cord mesenchymal stem cell-derived sEVs prompts peripheral nerve injury repair.

Repair and regeneration of the peripheral nerve are important for the treatment of peripheral nerve injury (PNI) caused by mechanical tears, external compression injuries and traction injuries. Pharmacological treatment can promote the proliferation of fibroblasts and Schwann cells (SCs), which longitudinally fill the endoneurial canal and form Bungner's band, helping the repair of peripheral nerves. Therefore, the development of new drugs for the treatment of PNI has become a top priority in recent years. Here, we report that small extracellular vesicles (sEVs) produced from umbilical cord mesenchymal stem cells (MSC-sEVs) cultured under hypoxia promote repair and regeneration of the peripheral nerve in PNI and may be a new therapeutic drug candidate. The results showed that the amount of secreted sEVs was significantly increased in UC-MSCs compared with control cells after 48 h of culture at 3% oxygen partial pressure in a serum-free culture system. The identified MSC-sEVs could be taken up by SCs in vitro, promoting the growth and migration of SCs. In a spared nerve injury (SNI) mouse model, MSC-sEVs accelerated the recruitment of SCs at the site of PNI and promoted peripheral nerve repair and regeneration. Notably, repair and regeneration in the SNI mouse model were enhanced by treatment with hypoxic cultured UC-MSC-derived sEVs. Therefore, we conclude that hypoxic cultured UC-MSC-derived sEVs may be a promising candidate drug for repair and regeneration in PNI.

Renal-friendly Li+-doped carbonized polymer dots activate Schwann cell autophagy for promoting peripheral nerve regeneration.

Activation of autophagy in Schwann cells (SCs) has emerged as a powerful trigger for peripheral nerve injury (PNI) repair. Lithium ion (Li+) is a classical autophagy activator that plays an important role in promoting axonal extension and remyelination. However, the therapeutic window of existing lithium drugs is extremely narrow, and the adverse side effects, especially nephrotoxicity, severely limit their therapeutic value. Herein, Li+-doped carbonized polymer dots (Li-CPDs) was synthesized for the first time to change the pharmacokinetics of Li+ from occupying epithelial sodium channels to lipid raft-mediated endocytosis. The in-vivo results confirmed that Li-CPDs could accelerate the removal of myelin debris and promote nerve regeneration via activating autophagy of SCs. Moreover, Li-CPDs exhibited almost no renal toxicity compared to that of raw lithium drugs. Thus, Li-CPDs could serve as a promising Li+-based nanomedicine for PNI regeneration with improved biosafety. STATEMENT OF SIGNIFICANCE: Regardless of the fact that lithium drugs have been used in treatment of mental illness such as manic depression, the systemic side effects and renal metabolic toxicity still seriously restrict their clinical application. Since Li+ and Na+ compete for ion channels of cell membrane, the cell entry efficiency is extremely low and easily affected by body fluctuations, which seems to be an unsolvable problem. Herein, we rationally exploited the endocytotic features of CPDs to develop Li-CPDs. The Li-CPDs improved the entry pathway, greatly reduced nephrotoxicity, and inherited the biological function of Li+ to activate autophagy for promoting peripheral nerve regeneration. Due to the BBB-crossing property of Li-CPDs, it also showed application prospects in future research on central nervous system diseases.

LncRNA HAGLR promotes the proliferation, migration, and neurotrophic factor production of Schwann cells via miR-204/CDK5R1 after sciatic nerve injury.

Peripheral nerve injury induces motor and sensory defects and has serious impacts on patients' quality of life. Schwann cells (SCs) are the major glial cells in the peripheral nervous system and play important roles in the repair and regeneration of peripheral nerves. Long noncoding RNA HAGLR has been reported to be highly expressed in neurons and to promote neuronal differentiation but its expression decreases after nerve injury, suggesting that HAGLR may be involved in the process of nerve injury repair. This study aimed to investigate the role and mechanism of HAGLR in neural repair functions of SCs. We found that HAGLR promoted SC proliferation and migration and facilitated the secretion of neurotrophic factors. Furthermore, HAGLR functions as a competing endogenous RNA to regulate CDK5R1 expression via sponging miR-204. Overexpression of miR-204 or silencing of CDK5R1 partially abolished the promoting effect of HAGLR on SCs. Moreover, overexpression of HAGLR promoted the functional recovery of sciatic nerve crush (SNC) model rats. In summary, HAGLR promoted SC proliferation, migration, neurotrophic factor production, and facilitated functional recovery of SNC rats via miR-204/CDK5R1. Therefore, it may provide a potential therapeutic target for peripheral nerve repair and regeneration.

Architecture-Engineered Electrospinning Cascade Regulates Spinal Microenvironment to Promote Nerve Regeneration.

The inflammatory cascade after spinal cord injury (SCI) causes necrotizing apoptosis of local stem cells, which limits nerve regeneration. Therefore, coordinating the inflammatory immune response and neural stem cell (NSC) functions is key to promoting the recovery of central nervous system function. In this study, a hydrogel "perfusion" system and electrospinning technology are integrated, and a "concrete" composite support for the repair of nerve injuries is built. The hydrogel's hydrophilic properties activate macrophage integrin receptors to mediate polarization into anti-inflammatory subtypes and cause a 10% increase in polarized M2 macrophages, thus reprogramming the SCI immune microenvironment. Programmed stromal cell-derived factor-1α and brain-derived neurotrophic factor released from the composite increase recruitment and neuronal differentiation of NSCs by approximately four- and twofold, respectively. The fiber system regulates the SCI immune inflammatory microenvironment, recruits endogenous NSCs, promotes local blood vessel germination and maturation, and improves nerve function recovery in a rat SCI model. In conclusion, the engineering fiber composite improves the local inflammatory response. It promotes nerve regeneration through a hydrophilic programmed cytokine-delivery system, which further improves and supplements the immune response mechanism regulated by the inherent properties of the biomaterial. The new fiber composite may serve as a new treatment approach for SCI.

Modulating axonal growth and neural stem cell migration with the use of uniaxially aligned nanofiber yarns welded with NGF-loaded microparticles

In tissue repair, cell behaviors can be modulated by sensing and responding to the topographical and biochemical cues provided by the surrounding microenvironment. Herein, we designed and fabricated a class of uniaxially aligned nanofiber yarns welded with electrosprayed microparticles to guide the directional growth of axons and the migration of neural stem cells. By tuning the depositing density of microparticles on the nanofiber yarns, the surface roughness was varied, which facilitated the directional axon outgrowth of PC12 and SH-SY5Y cells and the alignment of Schwann cells. The microparticles were further modified by loading nerve growth factors in the core and then deposited on the nanofiber yarns. Owing to the synthetic effects provided by the physical and biological signals, the migration of neural stem cells was significantly accelerated. Taken together, the uniaxially aligned nanofiber yarns welded by functionalized microparticles show promising use in manipulating axonal growth and the migration of neural stem cells, which will provide a novel approach to clinical repair of nerve injuries.

Platelet-Rich Plasma Gel-Loaded Collagen/Chitosan Composite Film Accelerated Rat Sciatic Nerve Injury Repair.

Peripheral nerve injury (PNI) is a common clinical disease caused by severe limb trauma, congenital malformations, and tumor resection, which may lead to significant functional impairment and permanent disability. Nerve conduit as a method for treating peripheral nerve injury shows good application prospects. In this work, the COL/CS composite films with different mass ratios of 1:0, 1:1, and 1:3 were fabricated by combining physical doping. Physicochemical characterization results showed that the COL/CS composite films possessed good swelling properties, ideal mechanical properties, degradability and suitable hydrophilicity, which could meet the requirements of nerve tissue engineering. In vitro cell experiments showed that the loading of platelet-rich plasma (PRP) gel on the surface of COL/CS composite films could significantly improve the biocompatibility of films and promote the proliferation of Schwann cells. In addition, a rat model of sciatic nerve defect was constructed to evaluate the effect of COL/CS composite films on peripheral nerve repair and the results showed that COL/CS composite films loaded with PRP gel could promote nerve regeneration and functional recovery in rats with sciatic nerve injury, indicating that the combination of PRP gel with the COL/CS composite film would be a potential approach for the treatment of peripheral nerve injury.

Perspectives on optimizing local delivery of drugs to peripheral nerves using mathematical models.

Drug therapies for treating peripheral nerve injury repair have shown significant promise in preclinical studies. Despite this, drug treatments are not used routinely clinically to treat patients with peripheral nerve injuries. Drugs delivered systemically are often associated with adverse effects to other tissues and organs; it remains challenging to predict the effective concentration needed at an injured nerve and the appropriate delivery strategy. Local drug delivery approaches are being developed to mitigate this, for example via injections or biomaterial-mediated release. We propose the integration of mathematical modeling into the development of local drug delivery protocols for peripheral nerve injury repair. Mathematical models have the potential to inform understanding of the different transport mechanisms at play, as well as quantitative predictions around the efficacy of individual local delivery protocols. We discuss existing approaches in the literature, including drawing from other research fields, and present a process for taking forward an integrated mathematical-experimental approach to accelerate local drug delivery approaches for peripheral nerve injury repair. This article is categorized under: Neurological Diseases > Molecular and Cellular Physiology Neurological Diseases > Computational Models Neurological Diseases > Biomedical Engineering.

Microfluidic Manipulation for Biomedical Applications in the Central and Peripheral Nervous Systems.

Physical injuries and neurodegenerative diseases often lead to irreversible damage to the organizational structure of the central nervous system (CNS) and peripheral nervous system (PNS), culminating in physiological malfunctions. Investigating these complex and diverse biological processes at the macro and micro levels will help to identify the cellular and molecular mechanisms associated with nerve degeneration and regeneration, thereby providing new options for the development of new therapeutic strategies for the functional recovery of the nervous system. Due to their distinct advantages, modern microfluidic platforms have significant potential for high-throughput cell and organoid cultures in vitro, the synthesis of a variety of tissue engineering scaffolds and drug carriers, and observing the delivery of drugs at the desired speed to the desired location in real time. In this review, we first introduce the types of nerve damage and the repair mechanisms of the CNS and PNS; then, we summarize the development of microfluidic platforms and their application in drug carriers. We also describe a variety of damage models, tissue engineering scaffolds, and drug carriers for nerve injury repair based on the application of microfluidic platforms. Finally, we discuss remaining challenges and future perspectives with regard to the promotion of nerve injury repair based on engineered microfluidic platform technology.

Bioengineered silkworm model for expressing human neurotrophin-4 with potential biomedical application.

Neurotrophin-4 (NT-4) is a neurotrophic factor that plays important roles in maintaining nerve cell survival, regulating neuronal differentiation and apoptosis, and promoting nerve injury repair. However, the source of sufficient NT-4 protein and efficient delivery of NT-4 remain a challenge. This study aims to express an activated human NT-4 protein in a large scale by genetically engineering silk gland bioreactor of silkworm as a host. We showed that the expression of human NT-4-functionalized silk material could promote proliferation of mouse HT22 cells when compared to the natural silk protein, and no obvious cytotoxicity was observed under the conditions of different silk materials. Importantly, this functional silk material was able to induce the potential differentiation of HT22 cells, promote peripheral neural cell migration and neurite outgrowth of chicken embryo dorsal root ganglion (DRG). All these results demonstrated a high bioactivity of human NT-4 protein produced in silk gland. Therefore, based on the silkworm model, the further fabrication of different silk materials-carrying active NT-4 protein with good mechanical properties and great biocompatibility will give promising applications in tissue engineering and neurons regeneration.

Long noncoding RNA Pvt1 promotes the proliferation and migration of Schwann cells by sponging microRNA-214 and targeting c-Jun following peripheral nerve injury.

Research has shown that long-chain noncoding RNAs (lncRNAs) are involved in the regulation of a variety of biological processes, including peripheral nerve regeneration, in part by acting as competing endogenous RNAs. c-Jun plays a key role in the repair of peripheral nerve injury. However, the precise underlying mechanism of c-Jun remains unclear. In this study, we performed microarray and bioinformatics analysis of mouse crush-injured sciatic nerves and found that the lncRNA Pvt1 was overexpressed in Schwann cells after peripheral nerve injury. Mechanistic studies revealed that Pvt1 increased c-Jun expression through sponging miRNA-214. We overexpressed Pvt1 in Schwann cells cultured in vitro and found that the proliferation and migration of Schwann cells were enhanced, and overexpression of miRNA-214 counteracted the effects of Pvt1 overexpression on Schwann cell proliferation and migration. We conducted in vivo analyses and injected Schwann cells overexpressing Pvt1 into injured sciatic nerves of mice. Schwann cells overexpressing Pvt1 enhanced the regeneration of injured sciatic nerves following peripheral nerve injury and the locomotor function of mice was improved. Our findings reveal the role of lncRNAs in the repair of peripheral nerve injury and highlight lncRNA Pvt1 as a novel potential treatment target for peripheral nerve injury.

Selective Repair of Motor Branches in the Femoral Nerve by Transferring the Motor Branches of Obturator Nerve: An Anatomical Feasibility Study.

Anterior branch of the obturator nerve transfer has been proven as an effective method for femoral nerve injuries, but the patient still has difficulty in rising and squatting, up and downstairs. Here, we presented a novel neurotization procedure of selectively repairing 3 motor branches of the femoral nerve by transferring motor branches of the obturator nerve in the thigh level and assessing its anatomical feasibility. Eight adult cadavers (16 thighs) were dissected. The nerve overlap distance between the gracilis branch and the rectus femoris (RF) branch, the adductor longus (AL) branch and the vastus medialis (VM) branch, as well as the adductor magnus (AM) branch and the vastus intermedius (VI) branch were measured. Also, the axon counts of the donor and recipient nerve were evaluated by histological evaluation. In all specimens, nerve overlap of at least 2.1 cm was observed in all 16 dissected thighs between the donor and recipient nerve branches, and the repair appeared to be without tension. There is no significant difference in the axon counts between gracilis branch (598 ± 83) and the RF branch (709 ± 151). The axon counts of the AL branch (601 ± 93) was about half of axon counts of the VM branch (1423 ± 189), and the axon counts of AM branch (761 ± 110) was also about half of the VI branch (1649 ± 281). This novel technique of the combined nerve transfers below the inguinal ligament, specifically the gracilis branch to the RF branch, the AL branch to the VM branch, and the AM branch to the VI branch, is anatomically feasible. It provides a promising alternative in the repair of femoral nerve injuries and an anatomical basis for the clinical application of motor branches of the obturator nerve transfer to repair the motor portion of the injured femoral nerve.

Artificial nerve graft constructed by coculture of activated Schwann cells and human hair keratin for repair of peripheral nerve defects.

Studies have shown that human hair keratin (HHK) has no antigenicity and excellent mechanical properties. Schwann cells, as unique glial cells in the peripheral nervous system, can be induced by interleukin-1β to secrete nerve growth factor, which promotes neural regeneration. Therefore, HHK with Schwann cells may be a more effective approach to repair nerve defects than HHK without Schwann cells. In this study, we established an artificial nerve graft by loading an HHK skeleton with activated Schwann cells. We found that the longitudinal HHK microfilament structure provided adhesion medium, space and direction for Schwann cells, and promoted Schwann cell growth and nerve fiber regeneration. In addition, interleukin-1β not only activates Schwann cells, but also strengthens their activity and increases the expression of nerve growth factors. Activated Schwann cells activate macrophages, and activated macrophages secrete interleukin-1β, which maintains the activity of Schwann cells. Thus, a beneficial cycle forms and promotes nerve repair. Furthermore, our studies have found that the newly constructed artificial nerve graft promotes the improvements in nerve conduction function and motor function in rats with sciatic nerve injury, and increases the expression of nerve injury repair factors fibroblast growth factor 2 and human transforming growth factor B receptor 2. These findings suggest that this artificial nerve graft effectively repairs peripheral nerve injury.

Adipose-derived stem cells and ginkgo biloba extract-loaded PCL/gelatin nanofibrous scaffolds for peripheral nerve injury repair: the impact of physical activity.

Peripheral nerve damages take place as a result of trauma, compression or disease, resulting in sensory loss, impaired motor function and subsequent challenges. In the current study, ginkgo biloba extract was loaded into PCL/gelatin scaffolds through electrospinning method. The scaffolds were characterized in vitro using various studies. The prepared nanofibrous scaffolds were rolled up to make neural guidance channels. Then, the conduits were seeded with adipose-derived stem cells and transplanted into a rat model of sciatic nerve injury. The scaffolds were not toxic and had optimal tensile and suturability. The animals treated with the conduits that delivered adipose-derived stem cells and ginkgo biloba extract, and received the treadmill exercise, had significantly higher motor and sensory functions recovery. In addition, histopathological examinations showed beneficial role of the exercise plan on the nervous system repair.

Hierarchically patterned protein scaffolds with nano-fibrillar and micro-lamellar structures modulate neural stem cell homing and promote neuronal differentiation.

Biophysical factors are essential in cell survival and behaviors, but constructing a suitable 3D microenvironment for the recruitment of stem cells and exerting their physiological functions remain a daunting challenge. Here, we present a novel silk fibroin (SF)-based fabrication strategy to develop hierarchical microchannel scaffolds for biomimetic nerve microenvironments in vitro. We first modulated the formation of SF nanofibers (SFNFs) that mimic the nanostructures of the native extracellular matrix (ECM) by using graphene oxide (GO) nanosheets as templates. Then, SFNF-GO systems were shaped into 3D porous scaffolds with aligned micro-lamellar structures by freeze-casting. The interconnected microchannels successfully induced cell infiltration and migration to the SFNF-GO scaffolds' interior. Meanwhile, the nano-fibrillar structures and the GO component significantly induced neural stem cells (NSCs) to differentiate into neurons within a short timeframe of 14 d. Importantly, these 3D hierarchical scaffolds induced a mild inflammatory response, extensive cell recruitment, and effective stimulation of NSC neuronal differentiation when implanted in vivo. Therefore, these SFNF-GO lamellar scaffolds with distinctive nano-/micro-topographies hold promise in the fields of nerve injury repair and regenerative medicine.

A Systematic Review and Meta-Analysis of Nerve Gap Repair: Comparative Effectiveness of Allografts, Autografts, and Conduits.

Ideal nerve repair involves tensionless direct repair, which may not be possible after resection. Bridging materials include nerve autograft, allograft, or conduit. This study aimed to perform a systematic literature review and meta-analysis to compare the meaningful recovery (MR) rates and postoperative complications following autograft, allograft, and conduit repairs in nerve gaps greater than 5 mm and less than 70 mm. A secondary aim was to perform a comparison of procedure costs. The search was conducted in MEDLINE from January of 1980 to March of 2020, following Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. Studies were included whether they reported nerve injury type, repair type, gap length, and outcomes for MR rates. Thirty-five studies with 1559 nerve repairs were identified. Overall MR for sensory and motor function was not significantly different between autograft ( n = 670) and allograft ( n = 711) across both short and long gaps. However, MR rates for autograft (81.6%) and allograft (87.1%) repairs were significantly higher compared with conduits (62.2%) ( P < 0.05) in sensory short gap repairs. Complication rates were comparable for autograft and allograft but higher for conduit with regard to pain. Analysis of costs showed that total costs for allograft repair were less than autograft in the inpatient setting and were comparable in the outpatient setting. Literature showed comparable rates of MR between autograft and allograft, regardless of gap length or nerve type. Furthermore, the rates of MR were lower in conduit repairs. In addition, the economic analysis performed demonstrates that allograft does not represent an increased economic burden compared with autograft.

AKBA Promotes Axonal Regeneration via RhoA/Rictor to Repair Damaged Sciatic Nerve.

The existing studies by our team demonstrated the pro-recovery effect of 3-Acetyl-11-keto-beta-boswellic acid (AKBA) on a sciatic nerve injury. To further investigate the role of AKBA in peripheral nerve injury repair, The TMT quantitative proteomics technique was used to obtain differentially significant proteins in a Sham group, Model group, and AKBA group. After that, three time points (5, 14, and 28 d) and four groups (Sham + AKBA, Sham, Model, and AKBA) were set up, and immunoblotting, immunofluorescence, and cellular assays were applied to investigate the expression of CDC42, Rac1, RhoA, and Rictor in the sciatic nerve at different time points for each group in more depth. The results showed that AKBA enriched the cellular components of the myelin sheath and axon regeneration after a sciatic nerve injury and that AKBA upregulated CDC42 and Rac1 and downregulated RhoA expression 5 d after a sciatic nerve injury, promoting axon regeneration and improving the repair of a sciatic nerve injury in rats. Rictor is regulated by AKBA and upregulated in PC12 cells after AKBA action. Our findings provide a new basis for AKBA treatment of a peripheral nerve injury.

Bioengineered nerve conduits and wraps for peripheral nerve repair of the upper limb

Bioengineered nerve conduits and wraps for peripheral nerve repair of the upper limb