Corrigendum:Resveratrol reduces brain injury after subarachnoid hemorrhage by inhibiting oxidative stress and endoplasmic reticulum stress

In the article titled“Resveratrol reduces brain injury after subarachnoid hemorrhage by inhibiting oxidative stress and endoplasmic reticulum stress”,published on pages 1734–1742,Issue 10,Volume 14 of Neural Regeneration Research(Xie et al.,2019),the author list is written incorrectly as“Yun-Kai Xie1,#,Xin Zhou1,2,#,Hong-Tao Yuan1,Jie Qiu1,Dan-Qing Xin1,Xi-Li Chu1,Da-Chuan Wang1,*,Zhen Wang2,*”instead of“Yun-Kai Xie1,#,Xin Zhou1,2,#,Hong-Tao Yuan1,Jie Qiu1,Dan-Qing Xin1,Xi-Li Chu1,Da-Chuan Wang2,*,Zhen Wang1,*”.     

Corrigendum:Glycogen synthase kinase-3β inhibitor SB216763 promotes DNA repair in ischemic retinal neurons

In the article titled“Glycogen synthase kinase-3βinhibitor SB216763 promotes DNA repair in ischemic retinal neurons”,published on pages 394–400,Issue 2,Volume 16 of Neural Regeneration Research(Zhang et al.,2021),there is an error in the author list.The author name Ying Yang was written incorrectly as Yang Ying.     

Correction Announcement

<正>The information of the first author Yanlin Bi of the article entitled"Adaptive and regulatory mechanisms in aged rats with postoperative cognitive dysfunc-tion"published in Neural Regeneration Research[2014;9(5):534-539]was mistaken during proofreading.The original information"Yanlin Bi1,2,Shuyun Liu2,Xinjuan Yu3,Mingshan Wu3,Yuelan Wang1"should be"Yanlin     

Absence of ephrin-A2/A3 increases retinal regenerative potential for Müller cells in Rhodopsin knockout mice

Müller cells(MC) are considered dormant retinal progenitor cells in mammals.Previous studies demonstrated ephrin-As act as negative regulators of neural progenitor cells in the retina and brain.It remains unclear whether the lack of ephrin-A2/A3 is sufficient to promote the neurogenic potential of MC.Here we investigated whether the MC is the primary retinal cell type expressing ephrin-A2/A3 and their role on the neurogenic potential of Müller cells.In this study, we showed that ephrin-A2/A3 and their receptor EphA4 were expressed in retina and especially enriched in MC.The level of ephrin As/EphA4 expression increased as the retina matured that is correlated with the reduced proliferative and progenitor cell potential of MC.Next, we investigated the proliferation in primary MC cultures isolated from wild-type and A2~(–/–) A3~(–/–) mice by 5-ethynyl-2′-deoxyuridine(EdU) incorporation.We detected a significant increase of EdU~+ cells in MC derived from A2~(–/–) A3~(–/–) mice.Next, we investigated the role of ephrin-A2/A3 in mice undergoing photoreceptor degeneration such as Rhodopsin knockout(Rho~(–/–)) mice.To further evaluate the role of ephrin-A2/A3 in MC proliferation in vivo, EdU was injected intraperitoneally to adult wild-type, A2~(–/–) A3~(–/–), Rho~(–/–) and Rho~(–/–) A2~(–/–) A3~(–/–) mice and the numbers of EdU~+ cells distributed among different layers of the retina.Ephrin As/EphA4 expression was upregulated in the retina of Rho~(–/–) mice compared to the wild-type mice.In addition, cultured MC derived from ephrin-A2~(–/–) A3~(–/–) mice also expressed higher levels of progenitor cell markers and exhibited higher proliferation potential than those from wild-type mice.Interestingly, we detected a significant increase of EdU~+ cells in the retinas of adult ephrin-A2~(–/–) A3~(–/–) mice mainly in the inner nuclear layer; and these EdU~+ cells were co-localized with MC marker, cellular retinaldehyde-binding protein, suggesting some proliferating cells are from MC.In Rhodopsin knockout mice(Rho~(–/–) A2~(–/–) A3~(–/–) mice), a significantly greater amount of EdU~+ cells were located in the ciliary body, retina and RPE than that of Rho~(–/–) mice.Comparing between 6 and 12 weeks old Rho~(–/–) A2~(–/–) A3~(–/–) mice, we recorded more EdU~+ cells in the outer nuclear layer in the 12-week-old mice undergoing severe retinal degeneration.Taken together, Ephrin-A2/A3 are negative regulators of the proliferative and neurogenic potentials of MC.Absence of ephrin-A2/A3 promotes the migration of proliferating cells into the outer nuclear layer and may lead to retinal cell regeneration.All experimental procedures were approved by the Animal Care and Use Committee at Schepens Eye Research Institute, USA(approval No.S-353-0715) on October 24, 2012.     

Nasal mucosal inhalation of amyloid-beta peptide 3–10 defective adenovirus attenuates cytotoxicity induced by beta-amyloid(1–42)

Three-month-old Alzheimer's disease model transgenic mice were immunized with Aβ1–42, Plp-Adenovirus [Ad]-X-CMV-(Aβ3–10)10-CpG [AdCpG-(Aβ3–10)10] or AdCpG virus fluid via nasal mucosal inhalation, respectively. ELISA analysis of serum showed Aβ42 antibody titers were significantly increased in mice immunized with Aβ1–42 and AdCpG-(Aβ3–10)10. Concanavalin A and AdCpG-(Aβ3–10)10 stimulation significantly increased the number of proliferating spleen cells cultured from AdCpG(Aβ3–10)10 and Aβ42 groups compared with the control group. In the AdCpG(Aβ3–10)10 group, levels of interleukin(IL)-4 and IL-10 were increased, while those of IL-2 and interferon-γ were decreased. In the Aβ42 group, levels of IL-4, IL-10, IL-2 and interferon-γ were all increased. Experimental findings indicate that AdCpG-(Aβ3–10)10 vaccine can produce strong T helper 2(Th2) humoral immune responses in addition to the production of Aβ42 antibody. The cellular immunologic response was weak and avoided Aβ1–42-mediated cytotoxicity.     

[Gly14]-Humanin Protects Against Amyloid β Peptide-Induced Impairment of Spatial Learning and Memory in Rats

Alzheimer disease（AD）, a progressive neurodegenerative disorder, is characterized by cognitive decline and the accumulation of senile plaques in the brain.Amyloid b protein（Aβ） in the plaques is thought to be responsible for the memory loss in AD patients. [Gly14]-humanin（HNG）, a derivative of humanin（HN）, has much stronger neuroprotective effects than natural HN in vitro.However, clarification of the Aβ active center and the neuroprotective mechanism of HN still need in vivo evidence. The present study first compared the in vivo biological effects of three Aβ fragments（1–42, 31–35, and 35–31） on spatial memory in rats, and investigated the neuroprotective effects and molecular mechanisms of HNG. The results showed that intrahippocampal injection of Aβ_1–42and Aβ_31–35almost equally impaired spatial learning and memory, but the reversed sequence Aβ_35–31 did not have any effect; a high dose of Aβ_31–35（20 nmol） produced a more detrimental response than a low dose（2 nmol）; Aβ_31–35 injection also disrupted gene and protein expression in the hippocampus, with up-regulation of caspase3 and down-regulation of STAT3; pretreatment with HNG not only protected spatial memory but also rescued STAT3 from Aβ-induced disruption; and the neuroprotective effects of HNG were effectively counteracted by genistein, a specific tyrosine kinase inhibitor. These results clearly show that sequence 31–35 in Aβ is the shortest active center responsible for the neurotoxicity of Aβ from molecule to behavior; and HNG protects spatial learning and memory in rats against Aβ-induced insults; and probably involves the activation of tyrosine kinases and subsequent beneficial modulation of STAT3 and caspase3.     

[Gly14]-Humanin Protects Against Amyloid b Peptide-Induced Impairment of Spatial Learning and Memory in Rats

Alzheimer disease(AD), a progressive neurodegenerative disorder, is characterized by cognitive decline and the accumulation of senile plaques in the brain.Amyloid b protein(Aβ) in the plaques is thought to be responsible for the memory loss in AD patients. [Gly14]-humanin(HNG), a derivative of humanin(HN), has much stronger neuroprotective effects than natural HN in vitro.However, clarification of the Aβ active center and the neuroprotective mechanism of HN still need in vivo evidence. The present study first compared the in vivo biological effects of three Aβ fragments(1–42, 31–35, and 35–31) on spatial memory in rats, and investigated the neuroprotective effects and molecular mechanisms of HNG. The results showed that intrahippocampal injection of Aβ_(1–42)and Aβ_(31–35)almost equally impaired spatial learning and memory, but the reversed sequence Aβ_(35–31) did not have any effect; a high dose of Aβ_(31–35)(20 nmol) produced a more detrimental response than a low dose(2 nmol); Aβ_(31–35) injection also disrupted gene and protein expression in the hippocampus, with up-regulation of caspase3 and down-regulation of STAT3; pretreatment with HNG not only protected spatial memory but also rescued STAT3 from Aβ-induced disruption; and the neuroprotective effects of HNG were effectively counteracted by genistein, a specific tyrosine kinase inhibitor. These results clearly show that sequence 31–35 in Aβ is the shortest active center responsible for the neurotoxicity of Aβ from molecule to behavior; and HNG protects spatial learning and memory in rats against Aβ-induced insults; and probably involves the activation of tyrosine kinases and subsequent beneficial modulation of STAT3 and caspase3.     

Corrigendum: Three-dimensional bioprinting collagen/silk fibroin scaffold combined with neural stem cells promotes nerve regeneration after spinal cord injury

doi:10.4103/1673-5374.280332 In the article titled“Three-dimensional bioprinting collagen/silk fibroin scaffold combined with neural stem cells promotes nerve regeneration after spinal cord injury”published on pages 959–968,Issue 5,Volume 15 of Neural Regeneration Research,(Jiang et al.,2020)the“author affiliations”are written incorrectly.The correct“author affiliations”are:“Ji-Peng Jiang1,#,Xiao-Yin Liu1,2,#,Fei Zhao1,#,Xiang Zhu3,Xiao-Yin Li1,Xue-Gang Niu4,Zi-Tong Yao1,Chen Dai1,Hui-You Xu1,Ke Ma1,Xu-Yi Chen1,*,Sai Zhang1,*1 Tianjin Key Laboratory of Neurotrauma Repair,Institute of Traumatic Brain Injury and Neuroscience,Center for Neurology and Neurosurgery of Chinese People’s Armed Police Force(PAP)Characteristic Medical Center,Tianjin,China;2 Tianjin Medical University,Tianjin,China;3 Department of Neurology,Luoyang First Hospital of Traditional Chinese Medicine,Luoyang,Henan Province,China;4 Department of Neurosurgery,Fourth Central Hospital of Tianjin,Tianjin,China.”     

Dynamic expression of Slit1–3 and Robo1–2 in the mouse peripheral nervous system after injury

The Slit family of axon guidance cues act as repulsive molecules for precise axon pathfinding and neuronal migration during nervous system development through interactions with specific Robo receptors.Although we previously reported that Slit1–3 and their receptors Robo1 and Robo2 are highly expressed in the adult mouse peripheral nervous system,how this expression changes after injury has not been well studied.Herein,we constructed a peripheral nerve injury mouse model by transecting the right sciatic nerve.At 14 days after injury,quantitative real-time polymerase chain reaction was used to detect mRNA expression of Slit1–3 and Robo1–2 in L4–5 spinal cord and dorsal root ganglia,as well as the sciatic nerve.Immunohistochemical analysis was performed to examine Slit1–3,Robo1–2,neurofilament heavy chain,F4/80,and vimentin in L4–5 spinal cord,L4 dorsal root ganglia,and the sciatic nerve.Co-expression of Slit1–3 and Robo1–2 in L4 dorsal root ganglia was detected by in situ hybridization.In addition,Slit1–3 and Robo1–2 protein expression in L4–5 spinal cord,L4 dorsal root ganglia,and sciatic nerve were detected by western blot assay.The results showed no significant changes of Slit1–3 or Robo1–2 mRNA expression in the spinal cord within 14 days after injury.In the dorsal root ganglion,Slit1–3 and Robo1–2 mRNA expression were initially downregulated within 4 days after injury;however,Robo1–2 mRNA expression returned to the control level,while Slit1–3 mRNA expression remained upregulated during regeneration from 4–14 days after injury.In the sciatic nerve,Slit1–3 and their receptors Robo1–2 were all expressed in the proximal nerve stump;however,Slit1,Slit2,and Robo2 were barely detectable in the nerve bridge and distal nerve stump within 14 days after injury.Slit3 was highly ex-pressed in macrophages surrounding the nerve bridge and slightly downregulated in the distal nerve stump within 14 days after injury.Robo1 was upregulated in vimentin-positive cells and migrating Schwann cells inside the nerve bridge.Robo1 was also upregulated in Schwann cells of the distal nerve stump within 14 days after injury.Our findings indicate that Slit3 is the major ligand expressed in the nerve bridge and distal nerve stump during peripheral nerve regeneration,and Slit3/Robo signaling could play a key role in peripheral nerve repair after injury.This study was approved by Plymouth University Animal Welfare Ethical Review Board (approval No.30/3203) on April 12,2014.     

Central projections and connections of lumbar primary afferent fibers in adult rats: effectively revealed using Texas red-dextran amine tracing

Signals from lumbar primary afferent fibers are important for modulating locomotion of the hind-limbs.However,silver impregnation techniques,autoradiography,wheat germ agglutinin-horseradish peroxidase and cholera toxin B subunit-horseradish peroxidase cannot image the central projections and connections of the dorsal root in detail.Thus,we injected 3-k Da Texas red-dextran amine into the proximal trunks of L4 dorsal roots in adult rats.Confocal microscopy results revealed that numerous labeled arborizations and varicosities extended to the dorsal horn from T12–S4,to Clarke's column from T10–L2,and to the ventral horn from L1–5.The labeled varicosities at the L4 cord level were very dense,particularly in laminae I–Ⅲ,and the density decreased gradually in more rostral and caudal segments.In addition,they were predominately distributed in laminae I–IV,moderately in laminae V–VⅡ and sparsely in laminae VⅢ–X.Furthermore,direct contacts of lumbar afferent fibers with propriospinal neurons were widespread in gray matter.In conclusion,the projection and connection patterns of L4 afferents were illustrated in detail by Texas red-dextran amine-dorsal root tracing.     

Nogo receptor expression in microglia/macrophages during experimental autoimmune encephalomyelitis progression

Myelin-associated inhibitory factors within the central nervous system(CNS) are considered to be one of the main obstacles for axonal regeneration following disease or injury. The nogo receptor 1(NgR1) has been well documented to play a key role in limiting axonal regrowth in the injured and diseased mammalian CNS. However, the role of nogo receptor in immune cell activation during CNS inflammation is yet to be mechanistically elucidated. Microglia/macrophages are immune cells that are regarded as pathogenic contributors to inflammatory demyelinating lesions in multiple sclerosis(MS). In this study, the animal model of MS, experimental autoimmune encephalomyelitis(EAE) was induced in ngr1~(+/+) and ngr1~(–/–) female mice following injection with the myelin oligodendrocyte glycoprotein(MOG_(35–55)) peptide. A fatemap analysis of microglia/macrophages was performed throughout spinal cord sections of EAE-induced mice at clinical scores of 0, 1, 2 and 3, respectively(increasing locomotor disability) from both genotypes, using the CD11 b and Iba1 cell markers. Western immunoblotting using lysates from isolated spinal cord microglia/macrophages, along with immunohistochemistry and flow cytometric analysis, was performed to demonstrate the expression of nogo receptor and its two homologs during EAE progression. Myelin protein engulfment during EAE progression in ngr1~(+/+) and ngr1~(–/–) mice was demonstrated by western immunblotting of lysates from isolated spinal cord microglia/macrophages, detecting levels of Nogo-A and MOG. The numbers of M1 and M2 microglia/macrophage phenotypes present in the spinal cords of EAE-induced ngr1~(+/+) and ngr1~(–/–) mice, were assessed by flow cytometric analysis using CD38 and Erg-2 markers. A significant difference in microglia/macrophage numbers between ngr1~(+/+) and ngr1~(–/–) mice was identified during the progression of the clinical symptoms of EAE, in the white versus gray matter regions of the spinal cord. This difference was unrelated to the expression of Ng R on these macrophage/microglial cells. We have identified that as EAE progresses, the phagocytic activity of microglia/macrophages with myelin debris, in ngr1~(–/–) mice, was enhanced. Moreover, we show a modulation from a predominant M1-pathogenic to the M2-neurotrophic cell phenotype in the ngr1~(–/–) mice during EAE progression. These findings suggest that CNS-specific macrophages and microglia of ngr1~(–/–) mice may exhibit an enhanced capacity to clear inhibitory molecules that are sequestered in inflammatory lesions.     

An Efficient and Reliable Assay for Investigating the Effects of Hypoxia/Anoxia on Drosophila

Stroke is a leading cause of death worldwide. Up to one thousand potential drugs or interventions have been developed to treat stroke, out of which ~160 have gone on to clinical trials. However, none of them has been successful. New insights into the molecular and cellular mechanisms of ischemia-induced injury are needed for discovering new therapeutic targets. Recently, Drosophila has been used to uncover new hypoxia-related genes. In this study, we describe an efficient and reliable assay with a sophisticated apparatus for studying the effects of oxygen deprivation on flies. Using this assay, wild-type flies were exposed to an anoxic environment for varying lengths of time, then the cumulative death rate and mobility recovery were systematically analyzed. We found that anoxia for over one hour caused lethality. The cumulative death rate on day 5 after anoxia was linearly and positively correlatedwith the duration of anoxia, and reached 50% when the duration was 2.5 h–3 h. We also found that the mobility recovery in normoxia was slow, as the climbing ability remained largely unchanged 4 h–6 h after 2.5-h of anoxia.We suggest that 2.5 h–3 h of anoxia and 4 h–6 h of recovery before mobility analysis are appropriate for future use of the anoxia assay.     

Altered Local Field Potential Relationship Between the Parafascicular Thalamic Nucleus and Dorsal Striatum in Hemiparkinsonian Rats

The thalamostriatal pathway is implicated in Parkinson's disease(PD); however, PD-related changes in the relationship between oscillatory activity in the centromedian-parafascicular complex(CM/Pf, or the Pf in rodents) and the dorsal striatum(DS) remain unclear.Therefore, we simultaneously recorded local field potentials(LFPs) in both the Pf and DS of hemiparkinsonian and control rats during epochs of rest or treadmill walking. The dopamine-lesioned rats showed increased LFP power in the beta band(12 Hz–35 Hz) in the Pf and DS during both epochs, but decreased LFP power in the delta(0.5 Hz–3 Hz) band in the Pf during rest epochs and in the DS during both epochs, compared to control rats. In addition,exaggerated low gamma(35 Hz–70 Hz) oscillations after dopamine loss were restricted to the Pf regardless of the behavioral state. Furthermore, enhanced synchronization of LFP oscillations was found between the Pf and DS after the dopamine lesion. Significant increases occurred in the mean coherence in both theta(3 Hz–7 Hz) and beta bands,and a significant increase was also noted in the phase coherence in the beta band between the Pf and DS during rest epochs. During the treadmill walking epochs, significant increases were found in both the alpha(7 Hz–12 Hz)and beta bands for two coherence measures. Collectively,dramatic changes in the relative LFP power and coherence in the thalamostriatal pathway may underlie the dysfunction of the basal ganglia-thalamocortical network circuits in PD, contributing to some of the motor and non-motor symptoms of the disease.     

High-frequency (50 Hz) electroacupuncture ameliorates cognitive impairment in rats with amyloid beta 1–42-induced Alzheimer's disease

Acupuncture has been shown to ameliorate cognitive impairment of Alzheimer’s disease.Acupoints and stimulation frequency influence the therapeutic effect of electroacupuncture.Rat models of Alzheimer’s disease were established by injecting amyloid beta 1–42(Aβ_(1–42))into the bilateral lateral ventricles.Electroacupuncture at 2,30,and 50 Hz was carried out at Baihui(GV20;15°obliquely to a depth of 2mm)and Shenshu(BL23;perpendicularly to 4–6 mm depth),once a day for 20 minutes(each),for 15 days,taking a break every 7 days.The Morris water maze test was conducted to assess the learning and memory.The expression levels of glycogen synthase kinase-3β(GSK-3β),p Ser9-GSK-3β,p Tyr216-GSK-3β,amyloid precursor protein and Aβ_(1–40) in the hippocampus were determined by western blot assay.Results demonstrated that electroacupuncture treatment at different frequencies markedly improved learning and memory ability,increased synaptic curvatures,decreased the width of synaptic clefts,thickened postsynaptic densities,and downregulated the expression of GSK-3β,amyloid precursor protein,and Aβ_(1–40).pSer9-GSK-3βexpression markedly decreased,while p Tyr216-GSK-3βexpression increased.High-frequency(50 Hz)electroacupuncture was more effective than low(2 Hz)or medium-frequency(30 Hz)electroacupuncture.In conclusion,electroacupuncture treatment exerts a protective effect against Aβ_(1–42)-induced learning and memory deficits and synapse-ultrastructure impairment via inhibition of GSK-3βactivity.Moreover,high-frequency electroacupuncture was the most effective therapy.     

Role of Notch-1 signaling pathway in PC12 cell apoptosis induced by amyloid beta-peptide(25–35)

Recent studies have demonstrated that Notch-1 expression is increased in the hippocampus of Alzheimer's disease patients. We speculate that Notch-1 signaling may be involved in PC12 cell apoptosis induced by amyloid beta-peptide(25–35)(Aβ25–35). In the present study, PC12 cells were cultured with different doses(0, 0.1, 1.0, 10 and 100 nmol/L) of N-[N-(3,5-Difluorophenacetyl)-L-alanyl]-S-phenylglycine t-butyl ester, a Notch-1 signaling pathway inhibitor, for 30 minutes. Then cultured cells were induced with Aβ25–35 for 48 hours. Pretreatment of PC12 cells with high doses of N-[N-(3,5-Difluorophenacetyl)-L-alanyl]-S-phenylglycine t-butyl ester( 10 nmol/L) prolonged the survival of PC12 cells after Aβ25–35 induction, decreased the expression of apoptosis-related proteins caspase-3,-8,-9, increased the activity of oxidative stress-related superoxide dismutase and catalase, inhibited the production of active oxygen, and reduced nuclear factor kappa B expression. This study indicates that the Notch-1 signaling pathway plays a pivotal role in Aβ25–35-induced PC12 apoptosis.     

Structure and function of the contactin-associated protein family in myelinated axons and their relationship with nerve diseases

The contactin-associated protein(Caspr) family participates in nerve excitation and conduction, and neurotransmitter release in myelinated axons. We analyzed the structures and functions of the Caspr family–CNTNAP1(Caspr1), CNTNAP2(Caspr2), CNTNAP3(Caspr3), CNTNAP4(Caspr4) and CNTNAP5(Caspr5), Caspr1–5 is not only involved in the formation of myelinated axons, but also participates in maintaining the stability of adjacent connections. Caspr1 participates in the formation, differentiation, and proliferation of neurons and astrocytes, and in motor control and cognitive function. We also analyzed the relationship between the Caspr family and neurodegenerative diseases, multiple sclerosis, and autoimmune encephalitis. However, the effects of Caspr on disease course and prognosis remain poorly understood. The effects of Caspr on disease diagnosis and treatment need further investigation.     

Jisuikang,a Chinese herbal formula,increases neurotrophic factor expression and promotes the recovery of neurological function after spinal cord injur y

The Chinese medicine compound, Jisuikang, can promote recovery of neurological function by inhibiting lipid peroxidation, scavenging oxygen free radicals, and effectively improving the local microenvironment after spinal cord injury. However, the mechanism remains unclear. Thus, we established a rat model of acute spinal cord injury using a modified version of Allen's method. Jisuikang(50, 25, and 12.5 g/kg/d) and prednisolone were administered 30 minutes after anesthesia. Basso, Beattie, and Bresnahan locomotor scale scores and the oblique board test showed improved motor function recovery in the prednisone group and moderate-dose Jisuikang group compared with the other groups at 3–7 days post-injury. The rats in the moderate-dose Jisuikang group recovered best at 14 days post-injury. Hematoxylin-eosin staining and transmission electron microscopy showed that the survival rate of neurons in treatment groups increased after 3–7 days of administration. Further, the structure of neurons and glial cells was more distinct, especially in prednisolone and moderate-dose Jisuikang groups. Western blot assay and immunohistochemistry showed that expression of brain-derived neurotrophic factor(BDNF) in injured segments was maintained at a high level after 7–14 days of treatment. In contrast, expression of nerve growth factor(NGF) was down-regulated at 7 days after spinal cord injury. Real-time fluorescence quantitative polymerase chain reaction showed that expression of BDNF and NGF m RNA was induced in injured segments by prednisolone and Jisuikang. At 3–7 days after injury, the effect of prednisolone was greater, while 14 days after injury, the effect of moderate-dose Jisuikang was greater. These results confirm that Jisuikang can upregulate BDNF and NGF expression for a prolonged period after spinal cord injury and promote repair of acute spinal cord injury, with its effect being similar to prednisolone.     

Exosome-mediated crosstalk between microglia and neural stem cells in the repair of brain injury

Brain injury,especially that caused by stroke,is a leading cause of morbidity and mortality worldwide.Numerous studies on the neuroprotective effects of neural stem cells(NSCs)after brain injury have shown that crosstalk among neural cells,including neuron–glial,glial–glial,NSC–neuronal and NSC–glial communication,plays a major role in post-injury repair.Therefore,a better understanding of the factors involved in the interactions between NSCs and other neural cells should advance the development of therapeutic strategies for brain injury.In this article,we discuss the role of exosomes in the crosstalk between NSCs and microglia,focusing on key exosomal proteins and microRNAs in brain injury progression and repair.