Research Progress on the Mechanism of Acupuncture Intervention on Alzheimer's Disease / 广州中医药大学学报

Alzheimer's disease(AD)is a multi-cause neurodegenerative disease characterized by memory impairment.There have been serious obstacles to the effective treatment of AD.Acupuncture,as a component of traditional Chinese medicine,plays an important role in the treatment of AD.Acupuncture has been shown to protect neurons from degeneration and promotes axonal regeneration in neurodegenerative diseases such as AD.According to existing studies,the mechanisms of acupuncture on AD include the following aspects:modulation of Aβ metabolism,tau phosphorylation,cholinergic neurotransmitters,neuroinflammation,synaptic and neuronal function,autophagy,brain glucose metabolism,intestinal flora,and inhibition of nerve cell apoptosis,which in turn improves cognition.

Paying attention to the basic research of optic nerve protection and regeneration, and promote its clinical transformation / 中华眼底病杂志

Primary or secondary death of retinal ganglion cells (RGC) is a common outcome in various optic neuropathies, often resulting in severe visual damage. The inherent characteristics of RGC include the continuous upregulation of intracellular growth-inhibitory transcription factors and the downregulation of growth-inducing transcription factors during cell differentiation. Additionally, the external inhibitory microenvironment following RGC damage, including oxidative stress, chronic inflammation, lack of neurotrophic factors, high expression of myelin proteins, and the formation of glial scars, all restrict axonal regeneration. Both intrinsic and extrinsic factors lead to the death of damaged RGC and hinder axonal regeneration. Various neuroprotective agents and methods attempt to promote neuroprotection and axonal regeneration from both intrinsic and extrinsic aspects, and well knowledge of these neuroprotective strategies is of significant importance for promoting the neuroprotective experimental research and facilitating its translation into clinical practice.

Recent advance in role of cAMP signaling pathway in axonal regeneration after peripheral nerve injury / 中华神经医学杂志

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.

Effects of delayed ramelteon treatment on neurological function and tissue repair after cryogenic traumatic brain injury / 中国药理学通报

:Aim To study the effects of continuous dai¬ly administration of ramelteon starting at the subacute period of cryogenic traumatic brain injury (cTBI) on neurological function and brain tissue repair in mice. Methods Thirty male C57BL/6 mice were randomly divided into sham group, vehicle group and ramelteon treatment groups. The right sensory-motor cortex was damaged by pressing a copper probe precooled by liq¬uid nitrogen onto the skull. Ramelteon ( 10 nig 'kg-1 • d"1) was administered by gavage every day starting at different time points after cTBI (1 h, 1 d,3 d) until sacrifice on day 14. Beam walking test and open field test were used to evaluate the motor function. Toluidine blue staining was used to measure the infarct volume. Immunofluorescence was used to detect the expression of GAP-43 and synaptophysin in peri-infarct area. Mi¬croglia activation was detected using Iba-1. The area and thickness of glial scars were analyzed by detecting GFAP positive areas. Results All three treatment ( 1 h - 14 d, 1 - 14 d, and 3 - 14 d) significantly im¬proved cTBI induced motor dysfunction, reduced the infarct volume, elevated the expression of GAP -43 and synaptophysin, and decreased the area and thick¬ness of glial scar and microglia activation. In addition, all ramelteon treatment groups had similar effects on the above indexes. Conclusions Delayed ramelteon treatment can improve neurological dysfunction after cTBI,and the therapeutic time window can be delayed for up to three days after cTBI. Inhibiting glial scar formation and microglia activation, and promoting ax- onal regeneration and synaptogenesis may contribute to the beneficial effects of ramelteon.

Effect of Buyang Huanwu Tang on Axonal Regeneration of Rats After Ischemic Stroke Injury / 中国实验方剂学杂志

Objective:To investigate the effects of Buyang Huanwu Tang （BHT） on axonal regeneration and neurological rehabilitation of the rats suffering ischemic stroke （IS）. Method:A total of 180 SD rats were used to establish a middle cerebral artery infarction （MCAO） model. The animals that were successfully modeled were randomly divided into model group， BHT group （12 g·kg-1） and nimodipine group （20 mg·kg-1）， and a sham group was established， with 28 rats in each group. After seven-days intragastric administration of BHT， the animals were sacrificed. TTC staining was used to test cerebral infarction. Brain water content was measured to observe cerebral edema. Bielschowsky's silver staining and immunofluorescence were performed to observe axonal degeneration and the protein expression of neurofilament protein-200（NF-200）. Quantitative real-time polymerase chain reaction （PCR） was used to analyze the mRNA expression of repulsion oriented molecule a （RGMa）， Ras homologous enzyme （Rho）， Rho kinase （ROCK）， and collapsion response regulatory protein 2 （CRMP2）. Neurological function scores assay was used to examine neurological recovery. Result:Compared with sham group， the cerebral infarction volume and brain water content increased significantly（P<0.01）， and motor function was markablely decreased in the model group. Axonal degeneration and nerve fiber damage were obviously observed. Also， gene expression of axon growth-related protein was deviation from normal （P<0.01）. Compared with model group， the cerebral infarction rate （P<0.01）， brain water content （P<0.01） and axonal degeneration of BHT group and nimodipine group were significantly reduced. The expression of NF-200 was increased. Also， the mRNA expression of RGMa， Rho and ROCK was lower （P<0.05） while the mRNA expression of CRMP2 was higher （P<0.01）. And the neurological function was significantly improved （P<0.05）. Conclusion:BHT can promote axon regeneration after ischemic stroke injury by regulating the mRNA expression of axon growth-related protein， thereby improving nerve function.

Effect of spinal cord decellularized scaffold on the repair of spinal cord defects in rats / 解剖学报

Objective Exploring the effect of spinal cord decellularized scaffold on spinal cord defects and observing the behavior and regeneration of rats after operation. Methods The spinal cords of 30 SD rats were treated with 3% Triton X-100 and 2% sodium deoxycholate on oscillator. The cell residue and the spatial structure of the tissue were compared before and after treatment, in order to understand the tissue structure of the stent itself. 90 SD rats were randomly divided into control group, simple injury group and stent transplantation group. Excision of the spinal cord 9-10 segments in the simple injury group and the stent graft group the acellular scaffold was transplanted to the stent graft group. Behavioral scores were observed postoperatively. At 4, 8, and 12 weeks, the spinal cords of the injured part of the rats were taken for HE staining and immunofluorescence detection of nerve regeneration-related proteins. Results After decellularization of the spinal cord, the nerve cells and axons were completely removed, and the extracellular matrix of the spinal cord was preserved. Scanning electron microscopy revealed that the scaffold retained a certain porous network scaffold structure. In the experiment of decellularized scaffold in vivo, the Basso-Beattie-Bresnahan(BBB) score showed that the recovery of hindlimb motor function in rats with decellularized scaffolds was better than that in rats with simple injury. HE staining showed that the decellularized scaffold could fill the defect of the spinal cord segment and accelerate the repair process of the injured spinal cord. Immunofluorescence showed that there was a certain axonal regeneration in the injured part of the stent transplantation group. Conclusion The spinal cord decellularized scaffold retains the extracellular matrix and has a certain spatial structure, which can accelerate the process of spinal cord defect repair to a certain extent, and has a certain promoting effect on nerve regeneration.

CaMKII-smad1 promotes axonal regeneration of peripheral nerves / 中国组织工程研究

BACKGROUND: Axons do not regenerate after central nervous system injury in mammals. It is mainly caused by the inhibitory microenvironment at the site of damage and the weakened self-regeneration ability. Studies have found that peripheral nervous system has certain regeneration ability after injury, so we explore the methods of central nervous system repair by studying the genes promoting peripheral nervous system regeneration. As one of the important protein kinase families of neurons, CaMKII up-regulation can improve the ability of neuron regeneration. Similarly, acute depletion of the Smad1 protein in adult mice also prevented axon regeneration in vivo. These genes can directly or indirectly regulate neuronal axon regeneration, but exactly how they regulate neuronal regeneration is still unclear. OBJECTIVE: To study the effects of CaMKII-Smad1 signaling pathway on axon regeneration of dorsal root ganglion neurons by intraperitoneal injection of CaMKII inhibitor and activator, and explored the mechanism of CaMKII and Smad1 in regulating axon regeneration of dorsal root ganglion neurons. METHODS: Totally 40 ICR mice were randomly divided into four groups: KN93 control group, KN93 experimental group, CdCl2 control group and CdCl2 experimental group. Dorsal root ganglion tissue was taken for in vitro culture after 7 days of continuous administration of CaMKII inhibitor KN93 and activator CdCl2. The length of axonal regeneration of dorsal root ganglion neurons was statistically analyzed after 3 days. Protein expression of p-Smad1 in dorsal root ganglion neurons was detected using western blot assay. RESULTS AND CONCLUSION: (1) Compared with the KN93 control group, axonal regeneration of dorsal root ganglion neurons was inhibited, and the p-Smad1 protein expression was decreased in the KN93 experimental group, showing significant differences. (2) Compared with the CdCl2 control group, axonal regeneration of dorsal root ganglion neurons was promoted, and p-Smad1 protein expression was increased in the CdCl2 experimental group, showing significant differences. (3) The results showed that the CaMKII-Smad1 signaling pathway had a regulatory effect on axonal regeneration of dorsal root ganglion neurons.

Investigation of axonal regeneration of Triturus ivanbureschi by using physiological and proteomic strategies

Peripheral nerve injuries are frequently observed and successful treatment depends mainly on the injury type, location of thedamage, and the elapsed time prior to treatment. The regenerative capacity is limited only to the embryonic period in manymammalian tissues, but urodele amphibians do not lose this feature during adulthood. The main purpose of this study is todefine the recovery period after serious sciatic nerve damage of a urodele amphibian, Triturus ivanbureschi. Experimentaltransection damage was performed on the sciatic nerves of T. ivanbureschi specimens. The recovery period of sciatic nerveswere investigated by walking track analysis, electrophysiological recordings, and bottom-up proteomic strategies at different time points during a 35-day period. A total of 34 proteins were identified related to the nerve regeneration process.This study showed that the expression levels of certain proteins differ between distal and proximal nerve endings during theregeneration period. In distal nerve stumps, transport proteins, growth factors, signal, and regulatory molecules are highlyexpressed, whereas in proximal nerve stumps, neurite elongation proteins, and cytoskeletal proteins are highly expressed.

Influence of exosome-derived miR-124 on molecular expression related to axonal regeneration after mechanical damage to cortical neurons in mice / 中华神经医学杂志

Objective To explore the influence of exosome-derived miR-124 on the molecular expression related to axonal regeneration after mechanical damage to cortical neurons in mice,aiming to provide experimental data for intervention in neurogenesis after traumatic brain injury (TBI).Methods The plasmid loaded with miR-124 was used to transfect the HEK293 cell line.The transfection effect was identified by real time Polymerase Chain Reaction (qPCR).The exosomes were isolated from the supematant of cultured transfected HEK293 cell line by the SBI isolation kit.The isolated exosomes were identified by electron microscopy and Western blotting,and the involved miR-124 in the exosomes was identified by qPCR.After the cortical neurons were isolated from the pregnant mice (14-17-day old) and cultured for 7 days,they were divided into 4 groups:control,damage,damage + exosomes without miR-124 and damage + exosomes with miR-124.The Petri dishes were manually scratched with a 10 μL plastic stylet needle to construct a mechanical damage in vitro in the latter 3 groups.The isolated exosomes without or with miR-124 were added into the cultured medium for culture for 72 h in the latter 2 groups,respectively.The expression ofmiR-124,NRP-1,Tau and Gap-43 was measured by qPCR and Western blotting respectively.Results The exosomes containing miR-124 were successfully obtained by plasmid transfection and the SBI isolation kit.The expression levels of miR-124,NRP-1 and Gap-43 in the damage + exosomes with miR-124 group were elevated significantly greater than in the other 3 groups (P＜0.05).The expression levels ofmiR-124,NRP-1 and Gap-43 in the damage group and damage + exosomes without miR-124 group were elevated significantly greater than in control group (P＜0.05).Conclusions The exosomes may transmit miR-124 to the cortical neurons in mice after mechanical damage and increase the expression ofmiR-124,NRP-1 and Gap-43 in the cortical neurons in mice.

The role of glial scar on axonal regeneration after spinal cord injury / 中国修复重建外科杂志

The 'glial scar' has been widely studied in the regeneration of spinal cord injury (SCI). For decades, mainstream scientific concept considers glial scar as a 'physical barrier' to impede axonal regeneration after SCI. Moreover, some extracellular molecules produced by glial scar are also regarded as axonal growth inhibitors. With the development of technology and the progress of research, multiple lines of new evidence challenge the pre-existing traditional notions in SCI repair, including the role of glial scar. This review briefly reviewed the history, advance, and controversy of glial scar research in SCI repair since 1930s, hoping to recognize the roles of glial scar and crack the international problem of SCI regeneration.

Salidroside regulates Akt/GSK-3β/CRMP-2expression and axonal regeneration in MCAO rats / 中国药理学通报

Aim To investigate the axonal regeneration effect of salidroside in MCAO rats and its potential mechanism.Methods Thirty-six healthy adult male Sprague-Dawley rats were randomly divided into three groups: sham, MCAO, MCAO+Sal groups.The rats were subjected to focal cerebral ischemia/reperfusion with suture-occluded method.Neurological deficit testing was performed with Zea Longa scale.The protein expression of p-Akt(Ser473), Akt, p-GSK-3β(Ser9), GSK-3β, p-CRMP-2(Thr514) and CRMP-2 in side cerebral ischemic tissues were determined using Western blot analysis.NF200 immunofluorescence staining was used to evaluate axonal regeneration.Results Compared with MCAO group,salidroside significantly improved the neurological deficit,up-regulated the protein expression of NF200,p-Akt and p-GSK-3β,and inhibited the protein expression of p-CRMP-2.Conclusions Salidroside improves neurological function recovery after focal cerebral/ischemic injury in rats,which may be associated with the up-regulation of phosphorylated Akt and GSK-3β and inhibition of phosphorylated CRMP-2,thereby promoting axonal regeneration.

Effect of Icariside Ⅱ on spatial learning and memory impairments and axonal regeneration in rats induced by chronic cerebral hypoperfusion / 中华行为医学与脑科学杂志

Objective To observe the effect of IcarisideⅡ (ICSⅡ) on spatial learning and memory impairments and axonal regeneration induced by chronic cerebral hypoperfusion (CCH) in rats.Methods 90 male SD rats were randomly divided into normal group,sham operation group,CCH group and ICS Ⅱ low,middle and high-dose treatment groups.The chronic cerebral hypoperfusion model was established by permanent bilateral common carotid artery occlusion.Then these rats in ICS Ⅱ low,middle and high-dose treatment groups were given ICS Ⅱ4,8 and 16 mg/(kg · d) by gavage on the 1st day after modeling.There were 5 rats in every group at each observing time(4,8 and 12 week).Morris water maze experiment was utilized to assess the escape latency and the target quadrant residence time while HE and immunohistochemistry analysis were applied to test the morphology change and expressions of GAP-43,MAP-2 and Nogo-A in hippocampal CA 1.Results Compared with those of sham operation groups at 4,8 and 12 week respectively,the escape latency in CCH group were significantly prolonged(40.02±4.95) s,(42.29±5.75) s,(53.68±6.14) s vs (26.43±2.68) s,(26.84±2.06) s,(31.53±4.12) s,P＜0.05;the target quadrant residence time were significantly reduced(28.53±2.40) s,(28.02±4.28) s,(22.60±4.03) s vs (33.34±2.89) s,(33.31 ±4.14) s,(31.63±2.20)s,P＜0.05);the expressions of GAP-43 and Nogo-A were increased with that of MAP-2 reduced(P＜0.05).Meanwhile,the neuropathological changes with more denatured neurons and less normal neurons were found in hippocampal CA1.However,compared with those of CCH group,the escape latency of ICS Ⅱ middle and high-dose groups (30.58±3.03) s,(29.19±4.23) s,(38.77±5.80) s;(28.90±2.98) s,(26.91 ±6.63) s,(36.51 ±3.98) s) were shortened (P＜0.05);the target quadrant residence time (32.54± 3.41) s,(32.69±3.47) s,(28.27±3.57) s;(32.69±3.54) s,(33.20±4.29) s,(28.07±4.04) s) were increased (P＜ 0.05);the expression of Nogo-A was decreased while those of GAP-43 and MAP-2 were conversely increased (P＜0.05).Moreover,few denatured neurons were observed in hippocampal CA1.But there were no differences for those indexs between CCH group and ICS Ⅱ low-dose treatment groups (P＞0.05).Compared with those in 8 week and 4 week,the escape latency and the target quadrant residence time were prolonged and reduced with the expression of Nogo-A increased in all groups except normal group and sham operation group(P＜0.05),the expressions of GAP-43 and MAP-2 were decreased in CCH group and ICS Ⅱ low-dose treatment group(P＜0.05),but there were no significant differences in ICS Ⅱ middle and high-dose treatment groups at 12 week(P＞0.05).However,there were no statistical significance of all indexes between 8 week and 4 week(P＞0.05).Conclusion ICS Ⅱ can improve the spatial learning and memory in chronic cerebral hypoperfusion rats,which may be achieved by neuroprotective effects and reducing the expression of Nogo-A consequently promotes the regeneration of axons.

PPE tube filled with autologous fat in the repair of peripheral nerve: a new proposal / Tubo PPE relleno con grasa autóloga en la reparación de los nervios periféricos: una nueva propuesta

This study proposes the use of a porous polyethylene (PPE) tube as the conductive element in the regeneration in the sciatic nerve sectioning and evaluates the use of fill with autologous fat. The subject was divided randomly into five groups, 3 control and 2 experimental (PPE tube graft with/ without autologous fat). Each group was selected for functional, histological and morphometric evaluation of the sciatic nerve. Functional analysis of the sciatic nerve occurred through the "footprint" values near -100 refer sectioned sciatic nerve, near 0 (zero) refer to control group. On histological analysis of the experimental groups lots of dense connective tissue replacing nerve tissue was observed. In morphometric analysis the group EGPGf got higher performance in all of variables. The use of PPE has shown promise in nerve regeneration with favorable results when associate with fat as a trophic factor in the regeneration.

Este estudio propone el uso de un tubo de polietileno poroso (PPE) como elemento conductor en la regeneración del nervio ciático seccionado y evaluar el uso de relleno con grasa autóloga. Al azar se formaron cinco grupos, 3 y 2 de control experimental (PPE prótesis tubular con / sin grasa autóloga). Cada grupo fue seleccionado para estudiar la forma funcional, histológica y evaluación morfométrica del nervio ciático. Un análisis funcional del nervio ciático se produjo a través de los valores de "huella", cerca de -100 se refiere al nervio ciático seccionado; cerca de 0 (cero) se refiere al grupo control. En el análisis histológico de los grupos experimentales se observó una gran cantidad de tejido conjuntivo denso que sustituye el tejido nervioso. En el análisis morfométrico, el grupo experimental de injerto de polietileno lleno de grasa (EGPGf) obtuvo un mayor rendimiento en todas las variables. El uso de PPE ha mostrado ser prometedor en la regeneración del nervio, con resultados favorables cuando se asocia con la grasa como un factor trófico en la regeneración.

Effect of Peripheral Nerve Electrical Stimulation on Axon Regeneration after Spinal Cord Injury in Rats / 中国康复理论与实践

Objective To explore the effect of peripheral nerve electrical stimulation on axon regeneration after spinal cord injury (SCI) in rats. Methods Nighty-two healthy Sprague-Dawley rats were randomly divided into blank control group (n=12), control group (n=40) and experimental group (n=40). All groups were suffered NYU impaction to prepare T8 SCI models, the control group and the experimental group implanted stimulating electrode on the sciatica nerve. The experimental group received electric intervention in addition. They were evaluated with BBB score one day, one week, two weeks, four weeks and eight weeks after modeling; and with motor evoked potentials (MEP) one week, two weeks, four weeks and eight weeks after modeling. Morphological changes and the expression of neurofilament pro-tein (NF)-200 and glial fibers acid protein (GFAP) were observed by HE staining and immunohistochemistry one week, two weeks, four weeks and eight weeks after modeling. Results There was no significant difference in BBB scores among three groups (P>0.05) in all the time points except eight weeks (P0.05), however, there was significant difference two weeks, four weeks and eight weeks after modeling (P0.05), but was different two weeks, four weeks and eight weeks after modeling (P0.05). Conclusion Implantable peripheral nerve electrical stimulation can improve conduction function and motor function in rats with SCI. And it may promote axonal regeneration of the injured segments.

Dynamic Expression of Nogo Receptor after Spinal Cord Injury in Rats / 中国康复理论与实践

Objective To observe the dynamic expression of Nogo receptor (NgR) in spinal cord of rats after spinal cord injury. Meth-ods 108 Sprague-Dawley rats were randomly assigned into normal group, sham operated group and model group, with 36 rats in each group. The model of spinal cord injury was established with the modified Allen's method. The rats were killed 24 h, 3 days, 7 days and 14 days re-spectively after intervention (9 rats from each group), and expression of NgR in the spinal cord tissue of the rats was detected with immuno-histochemistry and Western blotting, and expression of NgR mRNA was detected with fluorescence quantitative PCR. Results There was no significant change in the expression of NgR in the normal group and the sham operated group (P>0.05). The expression of protein and mRNA of NgR was less in the model group 24 h after modeling, dropped to the lowest on the 3rd day, then rapidly peaked on the 7th day, and gradually declined on the 14th day after spinal cord injury. Compared with the normal group, there were significant differences in ex-pression of NgR in immunohistochemistry and Western blotting in the model group at each time point after spinal cord injury (P<0.05). Compared with the sham operated group, there were significant differences in expression of NgR mRNA in the model group at each time point after spinal cord injury (P<0.01). Conclusion The expression of NgR and mRNA peaks on the 7th day after spinal cord injury in the rats, and maintains at high level for a long time, which may associated with the difficulty of axonal regeneration after spinal cord injury.

Aucubin Promotes Neurite Outgrowth in Neural Stem Cells and Axonal Regeneration in Sciatic Nerves

Aucubin is an iridoid glycoside with a wide range of biological activities, including anti-inflammatory, anti-microbial, anti-algesic as well as anti-tumor activities. Recently, it has been shown that aucubin prevents neuronal death in the hippocampal CA1 region in rats with diabetic encephalopathy. In addition, it has protective effects on H2O2-induced apoptosis in PC12 cells. We have shown here that aucubin promotes neuronal differentiation and neurite outgrowth in neural stem cells cultured primarily from the rat embryonic hippocampus. We also investigated whether aucubin facilitates axonal elongation in the injured peripheral nervous system. Aucubin promoted lengthening and thickness of axons and re-myelination at 3 weeks after sciatic nerve injury. These results indicate that administration of aucubin improved nerve regeneration in the rat model of sciatic nerve injury, suggesting that aucubin may be a useful therapeutic compound for the human peripheral nervous system after various nerve injuries.

Effect of Jisuikang on Neural Functional Recovery and Expression of Brain-derived Neurotrophic Factor after Spinal Cord Injury in Rats / 中国康复理论与实践

Objective To explore the effect of Jisuikang on neural functional recovery, and expression of brain-derived neurotrophic fac-tor (BDNF) protein and mRNA level after spinal cord injury (SCI). Methods 144 female Sprague-Dawley rats, weighted 180 to 220 g, were used for experiment. 24 rats were randomly extracted into sham group (Group A), which had their vertebral plates and spines bitten away on-ly. The others were randomly divided into model group (Group B), prednison group (Group C), and high, middle and low doses of Jisuikang group (Groups D to F) after SCI, 24 rats in each group. Group C was given 0.06 g/(kg?d) prednison, and Groups D to F were given 50, 25 and 12.5 g/(kg?d) Jisuikang respectively, which were given 20 ml/(kg?d) volume by intragastric administration. Groups A and B were given the same volume of normal saline (NS). The Basso-Beattie-Bresnahan (BBB) scores and oblique board test were applied to test the postoper-ative results 24 hours, 3, 7 and 14 days after SCI. The rats were executed and the spinal cord tissues were extracted 3, 7 and 14 days after SCI. Immunohistochemistry, Western blotting and RQ-PCR were applied to test the expression of protein and mRNA of BDNF. Results BBB scores and angle of oblique board test were significantly lower in Groups B to F than in Group A 24 hours after SCI (P0.05). The results of RQ-PCR showed that prednisone and Jisuikang promot-ed the expression of BDNF mRNA. Group C (prednisone) had a most obvious effect at the beginning while Group E was better than Group C 14 days after SCI. Conclusion Jisuikang can promote the neural functional recovery and the expression of BDNF on both protein and mRNA level in SCI rats.

Role of Glial Cells in Axonal Regeneration

Axonal regeneration is critical for functional recovery following neural injury. In addition to intrinsic differences between regenerative responses of axons in peripheral versus central nervous systems, environmental factors such as glial cells and related molecules in the extracellular matrix (ECM) play an important role in axonal regeneration. Schwann cells in the peripheral nervous system (PNS) are recognized as favorable factors that promote axonal regeneration, while astrocytes and oligodendrocytes in the central nervous system (CNS) are not. In this review, we evaluate the roles of Schwann cells and astrocytes in axonal regeneration and examine recent evidence that suggests a dual function of astrocytes in regenerative responses. We also discuss the role of Cdc2 pathways in axonal regeneration, which is commonly activated in Schwann cells and astrocytes. Greater insight on the roles of glial cells in axonal regeneration is key to establishing baseline interventions for improving functional recovery following neural injury.

Degeneration of peripheral nerves and expression changes of microtubule-associated protein 1B in rats after chronic spinal cord compression / 中华神经医学杂志

Objective To observe the morphological changes of the peripheral nerves,the expression changes of microtubule-associated protein 1B (MAP1B) and the changes of motor function in rats after chronic spinal cord compression.Methods A total of 50 female Wistar rats were randomly divided into normal control group (n=10),sham-operated group (n=10) and chronic compressive groups (n=30).The rats in the chronic compressive groups were given gradual compression on the posterior spinal cord using blunt plastics screw; compression degree reached 20％ (n=10),40％ (n=10) and 60％ (n=10),respectively,after 2 months.Rats in the normal control group did not receive any treatment and rats in the sham-operated group was only given removal of the L5 spinous process and part of the vertebral plate.Following sacrifice of the rats,cells from sciatic nerves were removed for HE staining;light microscopy and electron microscopy were employed to observe the changes; immunohistochemical staining of MAP1B was performed.Results Hypokinesia,and decreased Tarlov scores,Ramp test scores and BBB-21 scores in the chronic compressive groups were noted as compared with those in the normal control group (P＜0.05).Peripheral nerve degeneration was noted in all the chronic compressive groups; the more severe the compression,the more significant the degeneration.Expression of MAP1B in the peripheral nerves of the chronic compressive groups was significantly down-regulated as compared with that in the normal control group (P＜0.05).Conclusion Spinal cord compressive injury can lead to peripheral nerve degeneration; and neuronal apoptosis and necrosis lead to rare axonal regeneration,which may be one of the important reasons that influences the neural function recovery after chronic spinal cord compression.

Change of serum Nogo-A protein in patients with acute closed brain injury / 上海交通大学学报（医学版）

Objective To investigate the change of serum Nogo-A protein in patients with acute closed brain injury, and explore its relationship with the severity of neuronal damage and prognosis. Methods Thirty-one patients with acute closed brain injury were enrolled. Venous blood samples (2 mL) were obtained 1, 3 and 5 d after injury. Serum concentrations of Nogo-A protein were determined by ELISA. Patients were divided into mild (n =7), moderate (n = 10) and severe (n = 14) injury groups according to Glasgow coma score (GCS), and were divided into favorable prognosis (n = 23) and poor prognosis (n = 8) groups according to Glasgow outcome score (GOS). Another 20 healthy adults were served as controls. Results The mass concentrations of serum Nogo-A protein in mild, moderate and severe injury groups 1, 3, 5 d after injury were significantly higher than those in control group (P < 0.01), and the mass concentrations of serum Nogo-A protein in moderate and severe injury groups 1, 3, 5 d after injury were significantly higher than those in mild injury group (P <0.05, P <0.01). The mass concentrations of serum Nogo-A protein 1, 3, 5 d after injury were significantly higher in poor prognosis group than those in favourable prognosis group (P < 0.01). Conclusion Serum Nogo-A protein level significantly increases after brain injury, and is related to the degree of injury and prognosis.