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| 1 | Electroacupuncture promotes peripheral nerve regeneration after facial nerve crush injury and upregulates the expression of glial cell-derived neurotrophic factor显示文摘The efficacy of electroacupuncture in the treatment of peripheral facial paralysis is known, but the specific mechanism has not been clarified. Glial cell-derived neurotrophic factor(GDNF) has been shown to protect neurons by binding to N-cadherin. Our previous results have shown that electroacupuncture could increase the expression of N-cadherin mRNA in facial neurons and promote facial nerve regeneration. In this study, the potential mechanisms by which electroacupuncture promotes nerve regeneration were elucidated through assessing the effects of electroacupuncture on GDNF and N-cadherin expression in facial motoneurons of rabbits with peripheral facial nerve crush injury. New Zealand rabbits were randomly divided into a normal group(normal control, n = 21), injury group(n = 45) and electroacupuncture group(n = 45). Model rabbits underwent facial nerve crush injury only. Rabbits in the electroacupuncture group received facial nerve injury, and then underwent electroacupuncture at Yifeng(TE17), Jiache(ST6), Sibai(ST2), Dicang(ST4), Yangbai(GB14), Quanliao(SI18), and Hegu(LI4; only acupuncture, no electrical stimulation). The results showed that in behavioral assessments, the total scores of blink reflex, vibrissae movement, and position of apex nasi, were markedly lower in the EA group than those in the injury group. Hematoxylin-eosin staining of the right buccinator muscle of each group showed that the cross-sectional area of buccinator was larger in the electroacupuncture group than in the injury group on days 1, 14 and 21 post-surgery. Toluidine blue staining of the right facial nerve tissue of each group revealed that on day 14 post-surgery, there was less axonal demyelination and fewer inflammatory cells in the electroacupuncture group compared with the injury group. Quantitative real time-polymerase chain reaction showed that compared with the injury group, N-cadherin mRNA levels on days 4, 7, 14 and 21 and GDNF mRNA levels on days 4, 7 and 14 were significantly higher in the electroacupuncture group. Western blot assay displayed that compared with the injury group, the expression of GDNF protein levels on days 7, 14 and 21 were significantly upregulated in the electroacupuncture group. The histology with hematoxylin-eosin staining and Nissl staining of brainstem tissues containing facial neurons in the middle and lower part of the pons exhibited that on day 7 post-surgery, there were significantly fewer apoptotic neurons in the electroacupuncture group than in the injury group. By day 21, there was no significantly difference in the number of neurons between the electroacupuncture and normal groups. Taken together, these results have confirmed that electroacupuncture promotes regeneration of peripheral facial nerve injury in rabbits, inhibits neuronal apoptosis, and reduces peripheral inflammatory response, resulting in the recovery of facial muscle function. This is achieved by up-regulating the expression of GDNF and N-cadherin in central facial neurons. | Jing Fei Lin Gao Huan-Huan Li Qiong-Lan Yuan Lei-Ji Li | 2019 | Neural Regeneration Research2019，14，4： | 22 |
| 2 | Neuroprotective effect of Notch pathway inhibitor DAPT against focal cerebral ischemia/reperfusion 3 hours before model establishment显示文摘As an inhibitor of the Notch signaling pathway, N-[N-(3,5-difluorohenacetyl)-l-alanyl]-S-phenylglycine tert-butyl ester(DAPT) may protect brain tissue from serious ischemic injury. This study aimed to explore neuroprotection by DAPT after cerebral ischemia/reperfusion(I/R) injury. DAPT was intraperitoneally injected 3 hours before the establishment of a focal cerebral I/R model in the right middle cerebral artery of obstructed mice. Longa scores were used to assess neurological changes of mice. Nissl staining and TdT-mediated dUTP-biotin nick-end labeling staining were used to examine neuronal damage and cell apoptosis in the right prefrontal cortex, while immunofluorescence staining was used to detect glial fibrillary acidic protein-and Notch1-positive cells. Protein expression levels of Hes1 and Hes5 were detected by western blot assay in the right prefrontal cortex. Our results demonstrated that DAPT significantly improved neurobehavioral scores and relieved neuronal morphological damage. DAPT decreased the number of glial fibrillary acidic protein-and Notch1-positive cells in the right prefrontal cortex, while also reducing the number of apoptotic cells and decreasing interleukin-6 and tumor necrosis factor-α contents, and simultaneously downregulating Hes1 and Hes5 protein expression. These findings verify that DAPT alleviates pathological lesions and strengthens the anti-inflammatory response after cerebral I/R injury. Thus, DAPT might be developed as an effective drug for the prevention of cerebral I/R injury. | Jun-Jie Wang Jun-De Zhu Xian-Hu Zhang Ting-Ting Long Guo Ge Yan Yu | 2019 | Neural Regeneration Research2019，14，3： | 17 |
| 3 | Exosomes as mediators of neuron-glia communication in neuroinflammation显示文摘In recent years,a type of extracellular vesicles named exosomes has emerged that play an important role in intercellular communication under physiological and pathological conditions.These nanovesicles (30–150 nm) contain proteins,RNAs and lipids,and their internalization by bystander cells could alter their normal functions.This review focuses on recent knowledge about exosomes as messengers of neuron-glia communication and their participation in the physiological and pathological functions in the central nervous system.Special emphasis is placed on the role of exosomes under toxic or pathological stimuli within the brain,in which the glial exosomes containing inflammatory molecules are able to communicate with neurons and contribute to the pathogenesis of neuroinflammation and neurodegenerative disorders.Given the small size and characteristics of exosomes,they can cross the blood-brain barrier and be used as biomarkers and diagnosis for brain disorders and neuropathologies.Finally,although the application potential of exosome is still limited,current studies indicate that exosomes represent a promising strategy to gain pathogenic information to identify therapeutically targets and biomarkers for neurological disorders and neuroinflammation. | María Pascual Francesc Ibánez Consuelo Guerri | 2020 | Neural Regeneration Research2020，15，5： | 14 |
| 4 | Hyodeoxycholic acid protects the neurovascular unit against oxygen-glucose deprivation and reoxygenation-induced injury in vitro显示文摘Calculus bovis is commonly used for the treatment of stroke in traditional Chinese medicine. Hyodeoxycholic acid(HDCA) is a bioactive compound extracted from calculus bovis. When combined with cholic acid, baicalin and jas-minoidin, HDCA prevents hypoxia-reoxygenation-induced brain injury by suppressing endoplasmic reticulum stress-mediated apoptotic signaling. However, the effects of HDCA in ischemic stroke injury have not yet been studied. Neurovascular unit(NVU) dysfunction occurs in ischemic stroke. Therefore, in this study, we investigated the effects of HDCA on the NVU under ischemic conditions in vitro. We co-cultured primary brain microvascular endothelial cells, neurons and astrocytes using a transwell chamber co-culture system. The NVU was pre-treated with 10.16 or 2.54 μg/mL HDCA for 24 hours before exposure to oxygen-glucose deprivation for 1 hour. The cell counting kit-8 assay was used to detect cell activity. Flow cytometry and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling were used to assess apoptosis. Enzyme-linked immunosorbent assay was used to measure the expression levels of inflammatory cytokines, including interleukin-1β, interleukin-6 and tumor necrosis factor-α, and neurotrophic factors, including brain-derived neurotrophic factor and glial cell line-derived neurotrophic factor. Oxidative stress-related factors, such as superoxide dismutase, nitric oxide, malondialdehyde and γ-glutamyltransferase, were measured using kits. Pretreatment with HDCA significantly decreased blood-brain barrier permeability and neuronal apoptosis, significantly increased transendothelial electrical resistance and γ-glutamyltransferase activity, attenuated oxidative stress damage and the release of inflammatory cytokines, and increased brain-derived neurotrophic factor and glial cell line-derived neurotrophic factor expression. Our findings suggest that HDCA maintains NVU morphological integrity and function by modulating inflammation, oxidation stress, apoptosis, and the expression of neurotrophic factors. Therefore, HDCA may have therapeutic potential in the clinical management of ischemic stroke. This study was approved by the Ethics Committee of Experimental Animals of Beijing University of Chinese Medicine(approval No. BUCM-3-2016040201-2003) in April 2016. | Chang-Xiang Li Xue-Qian Wang Fa-Feng Cheng Xin Yan Juan Luo Qing-Guo Wang | 2019 | Neural Regeneration Research2019，14，11： | 13 |
| 5 | Neural crest derived stem cells from dental pulp and tooth-associated stem cells for peripheral nerve regeneration显示文摘The peripheral nerve injuries,representing some of the most common types of traumatic lesions affecting the nervous system,are highly invalidating for the patients besides being a huge social burden.Although peripheral nervous system owns a higher regenerative capacity than does central nervous system,mostly depending on Schwann cells intervention in injury repair,several factors determine the extent of functional outcome after healing.Based on the injury type,different therapeutic approaches have been investigated so far.Nerve grafting and Schwann cell transplantation have represented the gold standard treatment for peripheral nerve injuries,however these approaches own limitations,such as scarce donor nerve availability and donor site morbidity.Cell based therapies might provide a suitable tool for peripheral nerve regeneration,in fact,the ability of different stem cell types to differentiate towards Schwann cells in combination with the use of different scaffolds have been widely investigated in animal models of peripheral nerve injuries in the last decade.Dental pulp is a promising cell source for regenerative medicine,because of the ease of isolation procedures,stem cell proliferation and multipotency abilities,which are due to the embryological origin from neural crest.In this article we review the literature concerning the application of tooth derived stem cell populations combined with different conduits to peripheral nerve injuries animal models,highlighting their regenerative contribution exerted through either glial differentiation and neuroprotective/neurotrophic effects on the host tissue. | Alessandra Pisciotta Laura Bertoni Antonio Vallarola Giulia Bertani Daniela Mecugni Gianluca Carnevale | 2020 | Neural Regeneration Research2020，15，3： | 10 |
| 6 | Effect of sevoflurane preconditioning on astrocytic dynamics and neural network formation after cerebral ischemia and reperfusion in rats显示文摘Astrocytes, the major component of blood-brain barriers, have presented paradoxical profiles after cerebral ischemia and reperfusion in vivo and in vitro. Our previous study showed that sevoflurane preconditioning improved the integrity of blood-brain barriers after ischemia and reperfusion injury in rats. This led us to investigate the effects of sevoflurane preconditioning on the astrocytic dynamics in ischemia and reperfusion rats, in order to explore astrocytic cell-based mechanisms of sevoflurane preconditioning. In the present study, 2,3,5-triphenyltetrazolium chloride staining and Garcia behavioral scores were utilized to evaluate cerebral infarction and neurological outcome from day 1 to day 3 after transient middle cerebral artery occlusion surgery. Using immunofluorescent staining, we found that sevoflurane preconditioning substantially promoted the astrocytic activation and migration from the penumbra to the infarct with microglial activation from day 3 after middle cerebral artery occlusion. The formation of astrocytic scaffolds facilitated neuroblasts migrating from the subventricular zone to the lesion sites on day 14 after injury. Neural networks increased in the infarct of sevoflurane preconditioned rats, consistent with decreased infarct volume and improved neurological scores after ischemia and reperfusion injury. These findings demonstrate that sevoflurane preconditioning confers neuroprotection, not only by accelerating astrocytic spatial and temporal dynamics, but also providing astrocytic scaffolds for neuroblasts migration to ischemic regions, which facilitates neural reconstruction after brain ischemia. | Qiong Yu Li Li Wei-Min Liang | 2019 | Neural Regeneration Research2019，14，2： | 10 |
| 7 | Brain-Derived Glia Maturation Factor b Participates in Lung Injury Induced by Acute Cerebral Ischemia by Increasing ROS in Endothelial Cells显示文摘Brain damage can cause lung injury. To explore the mechanism underlying the lung injury induced by acute cerebral ischemia(ACI), we established a middle cerebral artery occlusion(MCAO) model in male Sprague-Dawley rats. We focused on glia maturation factor b(GMFB) based on quantitative analysis of the global rat serum proteome.Polymerase chain reaction, western blotting, and immunofluorescence revealed that GMFB was overexpressed in astrocytes in the brains of rats subjected to MCAO. We cultured rat primary astrocytes and confirmed that GMFB was also up-regulated in primary astrocytes after oxygen-glucose deprivation(OGD). We subjected the primary astrocytes to Gmfb RNA interference before OGD and collected the conditioned medium(CM) after OGD.We then used the CM to culture pulmonary microvascular endothelial cells(PMVECs) acquired in advance and assessed their status. The viability of the PMVECs improved significantly when Gmfb was blocked. Moreover,ELISA assays revealed an elevation in GMFB concentration in the medium after OGD. Cell cultures containing recombinant GMFB showed increased levels of reactive oxygen species and a deterioration in the state of the cells.In conclusion, GMFB is up-regulated in astrocytes after ACI, and brain-derived GMFB damages PMVECs by increasing reactive oxygen species. GMFB might thus be an initiator of the lung injury induced by ACI. | Fei-Fei Xu Zi-Bin Zhang Yang-Yang Wang Ting-Hua Wang | 2018 | Neuroscience Bulletin2018，34，6： | 7 |
| 8 | Neural stem cell transplantation inhibits glial cell proliferation and P2X receptor-mediated neuropathic pain in spinal cord injury rats显示文摘P2X4 and P2X7 receptors play an important role in neuropathic pain after spinal cord injury. Regulation of P2X4 and P2X7 receptors can obviously reduce pain hypersensitivity after injury. To investigate the role of neural stem cell transplantation on P2X receptor-mediated neuropathic pain and explore related mechanisms, a rat model of spinal cord injury was prepared using the free-falling heavy body method with spinal cord segment 10 as the center. Neural stem cells were injected into the injured spinal cord segment using a micro-syringe. Expression levels of P2X4 and P2X7 receptors, neurofilament protein, and glial fibrillary acidic protein were determined by immunohistochemistry and western blot assay. In addition, sensory function was quantitatively assessed by current perception threshold. The Basso-Beattie-Bresnahan locomotor rating scale was used to assess neuropathological pain. The results showed that 4 weeks after neural stem cell transplantation, expression of neurofilament protein in the injured segment was markedly increased, while expression of glial fibrillary acidic protein and P2X4 and P2X7 receptors was decreased. At this time point, motor and sensory functions of rats were obviously improved, and neuropathic pain was alleviated. These findings demonstrated that neural stem cell transplantation reduced overexpression of P2X4 and P2X7 receptors, activated locomotor and sensory function reconstruction, and played an important role in neuropathic pain regulation after spinal cord injury. Therefore, neural stem cell transplantation is one potential option for relieving neuropathic pain mediated by P2X receptors. | Xiao-Jing Du Yue-Xia Chen Zun-Cheng Zheng Nan Wang Xiao-Yu Wang Fan-E Kong | 2019 | Neural Regeneration Research2019，14，5： | 6 |
| 9 | Cytoprotective Mechanism of the Novel Gastric Peptide BPC157 in Gastrointestinal Tract and Cultured Enteric Neurons and Glial Cells显示文摘Dear Editor,Body protection compound (BPC) 157 is a stable gastric pentadecapeptide. Predrag Sikiric’s team has carried out many investigations of its cytoprotective effects in different organs and tissues (1, 2)Their evidence indicates that BPC157 has potent cytoprotection in neural injury and gastrointestinal (GI) ulcers. Nevertheless. | Xi-Yu Wang Meihua Qu Rui Duan Dengping Shi Ling Jin Jinping Gao Jackie D.Wood Junhua Li Guo-Du Wang | 2019 | Neuroscience Bulletin2019，35，1： | 6 |
| 10 | Use of a combination strategy to improve neuroprotection and neuroregeneration in a rat model of acute spinal cord injury显示文摘Spinal cord injury is a very common pathological event that has devastating functional consequences in patients. In recent years, several research groups are trying to find an effective therapy that could be applied in clinical practice. In this study, we analyzed the combination of different strategies as a potential therapy for spinal cord injury. Immunization with neural derived peptides(INDP), inhibition of glial scar formation(dipyridyl: DPY), as well as the use of biocompatible matrix(fibrin glue: FG) impregnated with bone marrow mesenchymal stem cells(MSCs) were combined and then its beneficial effects were evaluated in the induction of neuroprotection and neuroregeneration after acute SCI. Sprague-Dawley female rats were subjected to a moderate spinal cord injury and then randomly allocated into five groups: 1) phosphate buffered saline; 2) DPY; 3) INDP + DPY; 4) DPY+ FG; 5) INDP + DPY + FG + MSCs. In all rats, intervention was performed 72 hours after spinal cord injury. Locomotor and sensibility recovery was assessed in all rats. At 60 days after treatment, histological examinations of the spinal cord(hematoxylin-eosin and Bielschowsky staining) were performed. Our results showed that the combination therapy(DPY+ INDP + FG+ MSCs) was the best strategy to promote motor and sensibility recovery. In addition, significant increases in tissue preservation and axonal density were observed in the combination therapy group. Findings from this study suggest that the combination theapy(DPY+ INDP + FG + MSCs) exhibits potential effects on the protection and regeneration of neural tissue after acute spinal cord injury. All procedures were approved by the Animal Bioethics and Welfare Committee(approval No. 178544; CSNBTBIBAJ 090812960)on August 15, 2016. | Elisa García Roxana Rodríguez-Barrera Vinnitsa Buzoianu-Anguiano Adrian Flores-Romero Emanuel Malagón-Axotla Marco Guerrero-Godinez Estefanía De la Cruz-Castillo Laura Castillo-Carvajal Monserrat Rivas-Gonzalez Paola Santiago-Tovar Ivis Morales Cesar Borlongan Antonio Ibarra | 2019 | Neural Regeneration Research2019，14，6： | 6 |
| 11 | Activation of mitogen-activated protein kinases in satellite glial cells of the trigeminal ganglion contributes to substance P-mediated inflammatory pain显示文摘Inflammatory orofacial pain,in which substance P (SP) plays an important role,is closely related to the cross-talk between trigeminal ganglion (TG) neurons and satellite glial cells (SGCs).SGC activation is emerging as the key mechanism underlying inflammatory pain through different signalling mechanisms,including glial fibrillary acidic protein (GFAP) activation,phosphorylation of mitogen-activated protein kinase (MAPK) signalling pathways,and cytokine upregulation.However,in the TG,the mechanism underlying SP-mediated orofacial pain generated by SGCs is largely unknown.In this study,we investigated whether SP is involved in inflammatory orofacial pain by upregulating interleukin (IL)-1β and tumour necrosis factor (TNF)-α from SGCs,and we explored whether MAPK signalling pathways mediate the pain process.In the present study,complete Freund’s adjuvant (CFA) was injected into the whisker pad of rats to induce an inflammatory model in vivo.SP was administered to SGC cultures in vitro to confirm the effect of SP.Facial expression analysis showed that pre-injection of L703,606 (an NK-1 receptor antagonist),U0126 (an inhibitor of MAPK/extracellular signal-regulated kinase [ERK] kinase [MEK] 1/2),and SB203580 (an inhibitor of P38) into the TG to induce targeted prevention of the activation of the NK-1 receptor and the phosphorylation of MAPKs significantly suppressed CFA-induced inflammatory allodynia.In addition,SP promoted SGC activation,which was proven by increased GFAP,p-MAPKs,IL-1β and TNF-α in SGCs under inflammatory conditions.Moreover,the increase in IL-1β and TNF-α was suppressed by L703,606,U0126 and SB203580 in vivo and in vitro.These present findings suggested that SP,released from TG neurons,activated SGCs through the ERK1/2 and P38 pathways and promoted the production of IL-1β and TNF-α from SGCs,contributing to inflammatory orofacial pain associated with peripheral sensitization. | Yanyan Zhang Ning Song Fei Liu Jiu Lin Mengke Liu Chaolan Huang Daqing Liao Cheng Zhou Hang Wang Jiefei Shen | 2019 | International Journal of Oral Science2019，11，3： | 6 |
| 12 | Pretreated Oenan the Javanica extract increases anti-inflammatory cytokines, attenuates gliosis, and protects hippocampal neurons following transient global cerebral ischemia in gerbils显示文摘Recently,we have reported that Oenanthe javanica extract(OJE)displays strong neuroprotective effect against ischemic damage after transient global cerebral ischemia.However,neuroprotective mechanisms of OJE have not been fully identified.Thus,this study investigated the neuroprotection of OJE in the hippocampal CA1 area and its anti-inflammatory activity in gerbils subjected to 5 minutes of transient global cerebral ischemia.We treated the animals by intragastrical injection of OJE(100 and 200 mg/kg)once daily for 1 week prior to transient global cerebral ischemia.Neuroprotection of OJE was observed by immunohistochemistry for neuronal nuclear antigen and histofluorescence staining for Fluoro-Jade B.Immunohistochemistry of glial fibrillary acidic protein and ionized calcium-binding adapter molecule 1 was done for astrocytosis and microgliosis,respectively.To investigate the neuroprotective mechanisms of OJE,we performed immunohistochemistry of tumor necrosis factor-alpha and interleukin-2 for pro-inflammatory function and interleukin-4 and interleukin-13 for anti-inflammatory function.When we treated the animals by intragastrical administration of 200 mg/kg of OJE,hippocampal CA1 pyramidal neurons were protected from transient global cerebral ischemia and cerebral ischemia-induced gliosis was inhibited in the ischemic hippocampal CA1 area.We also found that interleukin-4 and-13 immunoreactivities were significantly increased in pyramidal neurons of the ischemic CA1 area after OJE pretreatment,and the increased immunoreactivities were sustained in the CA1 pyramidal neurons after transient global cerebral ischemia.However,OJE pretreatment did not increase interleukin-2 and tumor necrosis factor-alpha immunoreactivities in the CA1 pyramidal neurons.Our findings suggest that pretreatment with OJE can protect neurons and attenuate gliosis from transient global cerebral ischemia via increasing expressions of interleukin-4 and-13.The experimental plan of this study was reviewed and approved by the Institutional Animal Care and Use Committee(IACUC)in Kangwon National University(approval No.KW-160802-1)on August 10,2016. | Joon Ha Park In Hye Kim Ji Hyeon Ahn YooHun Noh Sung-Su Kim Tae-Kyeong Lee Jae-Chul Lee Bich-Na Shin Tae Heung Sim Hyun Sam Lee Jeong Hwi Cho In Koo Hwang Il Jun Kang Jong Dai Kim Moo-Ho Won | 2019 | Neural Regeneration Research2019，14，9： | 6 |
| 13 | Effect of preemptive local injection of ropivocaine with dexmedetomidine on mirror pain in rats and its mechanism显示文摘Objective:To observe the effect of preemptive local injection of ropivocaine with dexmedetomidine on activation of glial cells and on the mirror pain in rats and its mechanism.Methods:A total of 48 adult male Sprague-Dawley rats(weighing 180 g-220 g)were included in the study and randomized into 3 groups,Group S,Group R,and Group RD,.A rat model of persistent postoperative pain evoked by skin/muscle incision and retraction was established in the three groups.Before procedures and nerve extraction,Group S(n=16)was injected 0.9%saline locally;Group R(n=16)was injected 0.5%ropivocaine locally,and Group RD,(n=16)was injected 0.5%ropivocaine in combined with 1μg dexmedetomidine locally.After the model being established in the three groups,8 rats were used for behavior test until 28 d,and dorsal root ganglions(DRGs)of the other 8 rats were harvested on the3 rd day after surgery.Immunofluorescent and transmission electron microscopy were used to observe the activation of glial cells in DRG,and the behavior test results in the three groups were compared.Results:The results showed that mechanical pain threshold in ipsilateral hindpaws of the Group S,Group R,Group RD,animals dropped to(3.640±1.963)g,(5.827±1.204)g,(7.482)±1.412 g at 3 d respectively;while in contralateral paws dropped to(7.100±1.789)g,(17.687±1.112)g,(16.213±1.345)g on the 3 d respectively.Immunofluorescent showed that the glial cells were activated in bilateral side DRG after surgery in 3 groups,but ipsilateral paws expressed more active glial cells than contralateral paws.Transmission electron microscopy showed that mitochondria swelling/vacuolization and lysosomes were more obvious in ipsilateral paws than contralateral paws,but Group RD,formula could reduce glial cells activity,mitochondria swelling/vacuolization and the amount of lysosomes.Conclusions:Local injection of ropivocaine and/or dexmedetomidine can effectively inhibit the activation of glial cells in DRG,mitigate the pathological changes of neuron in DRG and reduce mirror image pain. | Xi-Zhao Huang Wei-Feng Tu Jie Peng Rong-Fang Deng Kai Mo Zu-Rong Hu Yi Lu | 2015 | Asian Pacific Journal of Tropical Medicine2015，8，10： | 6 |
| 14 | Differentiation of GDNF and NT-3 Dual Gene-modified Rat Bone Marrow Mesenchymal Stem Cells into Enteric Neuron-like Cells显示文摘Bone marrow mesenchymal stem cells (BMSCs) have been shown to be multipotent cells that possess high self-replicating capacity.The purpose of our study was to investigate the feasibility of using enteric neuron-like cells obtained by in vitro induction and differentiated from rat BMSCs for the treatment of Hirschsprung's disease (HD).Glial cell-derived neurotrophic factor (GDNF) and neurotrophin-3 (NT-3) are neurotrophic factors that play important roles in neuronal development,differentiation,survival and function.Meanwhile,GDNF mutations are a major cause of HD.In this study,BMSCs were transfected with eukaryotic expression plasmids co-expressing GDNF and NT-3,and the trans-fected cells displayed neuron-like changes after differentiation induced by fetal gut culture medium (FGCM).Immunofluorescence assay showed positive expression of the neuronal marker NSE and the enteric neuronal markers PGP9.5,VIP and nNOS.Reverse transcription-polymerase chain reaction (RT-PCR) revealed the expression of GDNF and NT-3 in transfected BMSCs.The present study indicates that genetically modified BMSCs coexpressing GDNF and NT-3 are able to differentiate into en-teric neuronal cells and express enteric nerve markers when induced by FGCM.This study provides an experimental basis for gene therapy to treat enteric nervous system-related disorders,such as HD. | 高贺云 魏明发 王燕 吴晓娟 朱天琦 | 2012 | Journal of Huazhong University of Science and Technology(Medical Sciences)2012，32，1： | 5 |
| 15 | Gene expression changes in dorsal root ganglia following peripheral nerve injury: roles in inflammation,cell death and nociception显示文摘Subsequent to a peripheral nerve injury, there are changes in gene expression within the dorsal root ganglia in response to the damage. This review selects factors which are well-known to be vital for inflammation, cell death and nociception, and highlights how alterations in their gene expression within the dorsal root ganglia can affect functional recovery. The majority of studies used polymerase chain reaction within animal models to analyse the dynamic changes following peripheral nerve injuries. This review aims to highlight the factors at the gene expression level that impede functional recovery and are hence are potential targets for therapeutic approaches. Where possible the experimental model, specific time-points and cellular location of expression levels are reported. | Sarah L.Martin Adam J.Reid Alexei Verkhratsky Valerio Magnaghi Alessandro Faroni | 2019 | Neural Regeneration Research2019，14，6： | 4 |
| 16 | PLZF^posc-KIT^pos-delineated A1-A4-differentiating spermatogonia by subset and stage detection upon Bouin fixation显示文摘While hallmarks of rodent spermatogonia stem cell biomarkers' heterogeneity have recently been identified, their stage and subset distributions remain unclear. Furthermore, it is currently difficult to accurately identify subset-specific SSC marker distributions due to the poor nuclear morphological characteristics associated with fixation in 4% paraformaldehyde. In the present study, testicular cross-sections and whole-mount samples were Bouin fixed to optimize nuclear resolution and visualized by immunohistochemistry (IHC) and immunofluorescence (IF). The results identified an expression pattern of PLZFhighc-KITpos in A1 spermatogonia, while A2–A4-differentiating spermatogonia were PLZFlowc-KITpos. Additionally, this procedure was used to examine asymmetrically expressing GFRA1 and PLZF clones, asymmetric Apr and false clones were distinguished based on the presence or absence of TEX14, a molecular maker of intercellular bridges, despite having identical nuclear morphology and intercellular distances that were <25 μm. In conclusion, this optimized Bouin fixation procedure facilitates the accurate identification of spermatogonium subsets based on their molecular profiles and is capable of distinguishing asymmetric and false clones. Therefore, the findings presented herein will facilitate further morphological and functional analysis studies and provide further insight into spermatogonium subtypes. | Rui-Ling Tang Li-Qing Fan | 2019 | Asian Journal of Andrology2019，21，3： | 3 |
| 17 | Regional brain susceptibility to neurodegeneration: what is the role of glial cells?显示文摘The main pathological feature of the neurodegenerative diseases is represented by neuronal death that represents the final step of a cascade of adverse/hostile events.Early in the neurodegenerative process,glial cells (including astrocytes,microglial cells,and oligodendrocytes) activate and trigger an insidious neuroinflammatory reaction,metabolic decay,blood brain barrier dysfunction and energy impairment,boosting neuronal death.How these mechanisms might induce selective neuronal death in specific brain areas are far from being elucidated.The last two decades of neurobiological studies have provided evidence of the main role of glial cells in most of the processes of the central nervous system,from development to synaptogenesis,neuronal homeostasis and integration into,highly specific neuro-glial networks.In this mini-review,we moved from in vitro and in vivo models of neurodegeneration to analyze the putative role of glial cells in the early mechanisms of neurodegeneration.We report changes of transcriptional,genetic,morphological,and metabolic activity in astrocytes and microglial cells in specific brain areas before neuronal degeneration,providing evidence in experimental models of neurodegenerative disorders,including Parkinson’s and Alzheimer’s diseases.Understanding these mechanisms might increase the insight of these processes and pave the way for new specific glia-targeted therapeutic strategies for neurodegenerative disorders. | Andrea Beatriz Cragnolini Giorgia Lampitella Assunta Virtuoso Immacolata Viscovo Fivos Panetsos Michele Papa Giovanni Cirillo | 2020 | Neural Regeneration Research2020，15，5： | 3 |
| 18 | Time-course pattern of neuronal loss and gliosis in gerbil hippocampi following mild, severe, or lethal transient global cerebral ischemia显示文摘Transient ischemia in the whole brain leads to neuronal loss/death in vulnerable brain regions. The striatum, neocortex and hippocampus selectively loose specific neurons after transient ischemia. Just 5 minutes of transient ischemia can cause pyramidal neuronal death in the hippocampal cornu ammonis (CA) 1 field at 4 days after transient ischemia. In this study, we investigated the effects of 5-minute (mild), 15-minute (severe), and 20-minute (lethal) transient ischemia by bilateral common carotid artery occlusion (BCCAO) on behavioral change and neuronal death and gliosis (astrocytosis and microgliosis) in gerbil hippocampal subregions (CA1-3 region and dentate gyrus). We performed spontaneous motor activity test to evaluate gerbil locomotor activity, cresyl violet staining to detect cellular distribution, neuronal nuclei immunohistochemistry to detect neuronal distribution, and Fluoro-Jade B histofluorescence to evaluate neuronal death. We also conducted immunohistochemical staining for glial fibrillary acidic protein and ionized calcium-binding adapter molecule 1 (Ibal) to evaluate astrocytosis and microgliosis, respectively. Animals subjected to 20-minute BCCAO died in at least 2 days. BCCAO for 15 minutes led to pyramidal cell death in hippocampal CA1-3 region 2 days later and granule cell death in hippocampal de匚tate gyrus 5 days later. Similar results were not found in animals subjected to 5-minute BCCAO. Gliosis was much more rapidly and severely progressed in animals subjected to 15-minute BCCAO than in those subjected to 5- minute BCCAO. Our results indicate that neuronal loss in the hippocampal formation following transient ischemia is significantly different according to regions and severity of transient ischemia. The experimental protocol was approved by Institutional Animal Care and Use Committee (AICUC) of Kangwon National University (approval No. KW-180124-1) on May 22, 2018. | Tae-Kyeong Lee Hyunjung Kim Minah Song Jae-Chul Lee Joon Ha Park Ji Hyeon Ahn Go Eun Yang Hyeyoung Kim Taek Geun Ohk Myoung Cheol Shin Jun Hwi Cho Moo-Ho Won | 2019 | Neural Regeneration Research2019，14，8： | 3 |
| 19 | Reliable cell purification and determination of cell purity:crucial aspects of olfactory ensheathing cell transplantation for spinal cord repair显示文摘Transplantation of olfactory ensheathing cells,the glia of the primary olfactory nervous system,has been trialed for spinal cord injury repair with promising but variable outcomes in animals and humans.Olfactory ensheathing cells can be harvested either from the lamina propria beneath the neuroepithelium in the nasal cavity,or from the olfactory bulb in the brain.As these areas contain several other cell types,isolating and purifying olfactory ensheathing cells is a critical part of the process.It is largely unknown how contaminating cells such as fibroblasts,other glial cell types and supporting cells affect olfactory ensheathing cell function post-transplantation;these cells may also cause unwanted side-effects.It is also,however,possible that the presence of some of the contaminant cells can improve outcomes.Here,we reviewed the last decade of olfactory ensheathing cell transplantation studies in rodents,with a focus on olfactory ensheathing cell purity.We analyzed how purification methods and resultant cell purity differed between olfactory mucosa-and olfactory bulb-derived cell preparations.We analyzed how the studies reported on olfactory ensheathing cell purity and which criteria were used to define cells as olfactory ensheathing cells.Finally,we analyzed the correlation between cell purity and transplantation outcomes.We found that olfactory bulb-derived olfactory ensheathing cell preparations are typically purer than mucosa-derived preparations.We concluded that there is an association between high olfactory ensheathing cell purity and favourable outcomes,but the lack of olfactory ensheathing cell-specific markers severely hampers the field. | Ronak Reshamwala Megha Shah Lucy Belt Jenny A.K.Ekberg James A.St John | 2020 | Neural Regeneration Research2020，15，11： | 3 |
| 20 | Multifunctional biomimetic spinal cord: New approach to repair spinal cord injuries显示文摘The incidence of spinal cord injury(SCI) has been gradually increasing, and the treatment has troubled the medical field all the time. Primary and secondary injuries ultimately lead to nerve impulse conduction block. Microglia and astrocytes excessively accumulate and proliferate to form the glial scar. At present, to reduce the effect of glial scar on nerve regeneration is a hot spot in the research on the treatment of SCI. According to the preliminary experiments, we would like to provide a new bionic spinal cord to reduce the negative effect of glial scar on nerve regeneration. In this hypothesis we designed a new scaffold that combine the common advantage of acellular scaffold of spinal cord and thermosensitive gel, which could continue to release exogenous basic fibroblast growth factor(BFGF) in the spinal lesion area on the basis of BFGF modified thermosensitive gel. Meanwhile, the porosity, pore size and material of the gray matter and white matter regions were distinguished by an isolation layer, so as to induce the directed differentiation of cells into the defect site and promote regeneration of spinal cord tissue. | Yang Liu Qian Li Bin Zhang De-Xiang Ban Shi-Qing Feng | 2017 | World Journal of Experimental Medicine2017，7，3： | 3 |
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