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| 1 | Autophagy and inflammation in ischemic stroke显示文摘Appropriate autophagy has protective effects on ischemic nerve tissue,while excessive autophagy may cause cell death.The inflammatory response plays an important role in the survival of nerve cells and the recovery of neural tissue after ischemia.Many studies have found an interaction between autophagy and inflammation in the pathogenesis of ischemic stroke.This study outlines recent advances regarding the role of autophagy in the post-stroke inflammatory response as follows.(1)Autophagy inhibits inflammatory responses caused by ischemic stimulation through mTOR,the AMPK pathway,and inhibition of inflammasome activation.(2)Activation of inflammation triggers the formation of autophagosomes,and the upregulation of autophagy levels is marked by a significant increase in the autophagy-forming markers LC3-II and Beclin-1.Lipopolysaccharide stimulates microglia and inhibits ULK1 activity by direct phosphorylation of p38 MAPK,reducing the flux and autophagy level,thereby inducing inflammatory activity.(3)By blocking the activation of autophagy,the activation of inflammasomes can alleviate cerebral ischemic injury.Autophagy can also regulate the phenotypic alternation of microglia through the nuclear factor-κB pathway,which is beneficial to the recovery of neural tissue after ischemia.Studies have shown that some drugs such as resveratrol can exert neuroprotective effects by regulating the autophagy-inflammatory pathway.These studies suggest that the autophagy-inflammatory pathway may provide a new direction for the treatment of ischemic stroke. | Yun Mo Yin-Yi Sun Kang-Yong Liu | 2020 | Neural Regeneration Research2020，15，8： | 90 |
| 2 | Angiogenesis and neuronal remodeling after ischemic stroke显示文摘Increased microvessel density in the peri-infarct region has been reported and has been correlated with longer survival times in ischemic stroke patients and has improved outcomes in ischemic animal models.This raises the possibility that enhancement of angiogenesis is one of the strategies to facilitate functional recovery after ischemic stroke.Blood vessels and neuronal cells communicate with each other using various mediators and contribute to the pathophysiology of cerebral ischemia as a unit.In this mini-review,we discuss how angiogenesis might couple with axonal outgrowth/neurogenesis and work for functional recovery after cerebral ischemia.Angiogenesis occurs within 4 to 7 days after cerebral ischemia in the border of the ischemic core and periphery.Post-ischemic angiogenesis may contribute to neuronal remodeling in at least two ways and is thought to contribute to functional recovery.First,new blood vessels that are formed after ischemia are thought to have a role in the guidance of sprouting axons by vascular endothelial growth factor and laminin/β1-integrin signaling.Second,blood vessels are thought to enhance neurogenesis in three stages:1)Blood vessels enhance proliferation of neural stem/progenitor cells by expression of several extracellular signals,2)microvessels support the migration of neural stem/progenitor cells toward the peri-infarct region by supplying oxygen,nutrients,and soluble factors as well as serving as a scaffold for migration,and 3)oxygenation induced by angiogenesis in the ischemic core is thought to facilitate the differentiation of migrated neural stem/progenitor cells into mature neurons.Thus,the regions of angiogenesis and surrounding tissue may be coupled,representing novel treatment targets. | Masahiro Hatakeyama Itaru Ninomiya Masato Kanazawa | 2020 | Neural Regeneration Research2020，15，1： | 63 |
| 3 | Autophagy: a double-edged sword for neuronal survival after cerebral ischemia显示文摘Evidence suggests that autophagy may be a new therapeutic target for stroke, but whether activation of autophagy increases or decreases the rate of neuronal death is still under debate. This review summarizes the potential role and possible signaling pathway of autophagy in neuronal survival after cerebral ischemia and proposes that autophagy has dual effects. | Wenqi Chen Yinyi Sun Kangyong Liu Xiaojiang Sun | 2014 | Neural Regeneration Research2014，9，12： | 57 |
| 4 | Knowledge domain and emerging trends in Alzheimer’s disease: a scientometric review based on CiteSpace analysis显示文摘Alzheimer’s disease is the most common cause of dementia.It is an increasingly serious global health problem and has a significant impact on individuals and society.However,the precise cause of Alzheimer’s disease is still unknown.In this study,11,748 Web-of-Science-indexed manuscripts regarding Alzheimer’s disease,all published from 2015 to 2019,and their 693,938 references were analyzed.A document co-citation network map was drawn using CiteSpace software.Research frontiers and development trends were determined by retrieving subject headings with apparent changing word frequency trends,which can be used to forecast future research developments in Alzheimer’s disease. | Shuo Liu Ya-Ping Sun Xu-Ling Gao Yi Sui | 2019 | Neural Regeneration Research2019，14，9： | 59 |
| 5 | Efficacy of cattle encephalon glycoside and ignotin in patients with acute cerebral infarction: a randomized, double-blind, parallel-group, placebo-controlled study显示文摘Cattle encephalon glycoside and ignotin(CEGI)injection is a compound preparation formed by a combination of muscle extract from hea lthy rabbits and brain gangliosides from cattle,and it is generally used as a neuroprotectant in the treatment of central and peripheral nerve injuries.However,there is still a need for high-level clinical evidence from large samples to support the use of CEGI.We therefore carried out a prospective,multicenter,randomized,double-blind,parallel-group,placebo-controlled study in which we recruited 319 patients with acute cerebral infarction from 16 centers in China from October 2013 to May 2016.The patients were randomized at a 3:1 ratio into CEGI(n=239;155 male,84 female;61.2±9.2 years old)and placebo(n=80;46 male,34 female;63.2±8.28 years old)groups.All patients were given standard care once daily for 14 days,including a 200 mg aspirin enteric-coated tablet and 20 mg atorvastatin calcium,both taken orally,and intravenous infusion of 250–500 mL 0.9%sodium chloride containing 40 mg sodium tanshinone IIA sulfonate.Based on conventional treatment,patients in the CEGI and placebo groups were given 12 mL CEGI or 12 mL sterile water,respectively,in an intravenous drip of 250 mL 0.9%sodium chloride(2 mL/min)once daily for 14 days.According to baseline National Institutes of Health Stroke Scale scores,patients in the two groups were divided into mild and moderate subgroups.Based on the modified Rankin Scale results,the rate of patients with good outcomes in the CEGI group was higher than that in the placebo group,and the rate of disability in the CEGI group was lower than that in the placebo group on day 90 after treatment.In the CEGI group,neurological deficits were decreased on days 14 and 90 after treatment,as measured by the National Institutes of Health Stroke Scale and the Barthel Index.Subgroup analysis revealed that CEGI led to more significant improvements in moderate stroke patients.No drug-related adverse events occurred in the CEGI or placebo groups.In conclusion,CEGI may be a safe and effective treatment for acute cerebral infarction patients,especially for moderate stroke patients.This study was approved by the Ethical Committee of Peking University Third Hospital,China(approval No.2013-068-2)on May 20,2013,and registered in the Chinese Clinical Trial Registry(registration No.ChiCTR1800017937). | Hui Zhang Chuan-Ling Li Feng Wan Su-Juan Wang Xiu-E Wei Yan-Lei Hao Hui-Lin Leng Jia-Min Li Zhong-Rui Yan Bao-Jun Wang Ren-Shi Xu Ting-Min Yu Li-Chun Zhou Dong-Sheng Fan | 2020 | Neural Regeneration Research2020，15，7： | 54 |
| 6 | Correlation of E-selectin gene polymorphisms with risk of ischemic stroke A meta-analysis显示文摘OBJECTIVE: To investigate the association of E-selectin S128R polymorphisms with ischemic stroke. DATA SOURCES: A computer-based online search was conducted in PubMed, Elsevier, Ovid Database, the China National Knowledge Infrastructure, and Wanfang Database between January 1998 and December 2010. STUDY SELECTION: Case-controlled studies addressing the association of the E-selectin polymorphism and ischemic stroke were included in this review. The genotype distribution complied with the Hardy-Weinberg genetic equilibrium. The included reports were evaluated by two authors for strict quality screening. Meta-analysis software, REVMAN 5.1, was used to investigate heterogeneity, pooled odds ratio (OR) and 95% confidence interval (CI) in individual studies. MAIN OUTCOME MEASURES: Genotype and allele distributions at the E-selectin S128R site. RESULTS: Six case-controlled studies were included after screening and application of inclusion and exclusion criteria. There was no heterogeneity in the genotype and allele frequencies, and no publication bias was found. Meta-analysis of the pooled data showed that the OR value of the (AC+CC)/AA genotype was 1.93 (95% CI: 1.55-2.41, Z = 5.80, P < 0.000 01), and the OR for the C/A allele was 1.80 (95% CI: 1.47-2.22, Z = 5.59, P < 0.000 01) in the ischemic stroke group, compared with control group. Results of pooled data in Chinese subjects showed that the OR value of (AC+CC)/AA was 2.36 (95% CI: 1.68-3.31, Z = 4.99, P < 0.000 01), and the OR value of the C/A allele was 2.25 (95% CI: 1.63-3.12, Z = 4.89, P < 0.000 01). CONCLUSION: Polymorphism of E-selectin S128R was significantly associated with susceptibility to ischemic stroke; the AC and CC genotypes as well as the C allele may be factors associated with susceptibility to ischemic stroke. | Qingli Sun Yu Fu Aping Sun Yanhong Shou Mei Zheng Xiaogang Li Dongsheng Fan | 2011 | Neural Regeneration Research2011，6，22： | 46 |
| 7 | 3-N-butylphthalide improves neuronal morphology after chronic cerebral ischemia显示文摘3-N-butylphthalide is an effective drug for acute ischemic stroke. However, its effects on chronic cerebral ischemia-induced neuronal injury remain poorly understood. Therefore, this study ligated bilateral carotid arteries in 15-month-old rats to simulate chronic cerebral ischemia in aged humans. Aged rats were then intragastrically administered 3-n-butylphthalide. 3-N-butylphthalide administration improved the neuronal morphology in the cerebral cortex and hippocampus of rats with chronic cerebral ischemia, increased choline acetyltransferase activity, and decreased malondialdehyde and amyloid beta levels, and greatly improved cognitive function. These findings suggest that 3-n-butylphthalide alleviates oxidative stress caused by chronic cerebral ischemia, improves cholinergic function, and inhibits amyloid beta accumulation, thereby improving cerebral neuronal injury and cognitive deficits. | Wanhong Zhao Chao Luo Jue Wang Jian Gong Bin Li Yingxia Gong Jun Wang Hanqin Wang | 2014 | Neural Regeneration Research2014，9，7： | 43 |
| 8 | Ligustrazine monomer against cerebral ischemia/reperfusion injury显示文摘Ligustrazine(2,3,5,6-tetramethylpyrazine) is a major active ingredient of the Szechwan lovage rhizome and is extensively used in treatment of ischemic cerebrovascular disease.The mechanism of action of ligustrazine use against ischemic cerebrovascular diseases remains unclear at present.This study summarizes its protective effect,the optimum time window of administration,and the most effective mode of administration for clinical treatment of cerebral ischemia/reperfusion injury.We examine the effects of ligustrazine on suppressing excitatory amino acid release,promoting migration,differentiation and proliferation of endogenous neural stem cells.We also looked at its effects on angiogenesis and how it inhibits thrombosis,the inflammatory response,and apoptosis after cerebral ischemia.We consider that ligustrazine gives noticeable protection from cerebral ischemia/reperfusion injury.The time window of ligustrazine administration is limited.The protective effect and time window of a series of derivative monomers of ligustrazine such as 2-[(1,1-dimethylethyl)oxidoimino]methyl]-3,5,6-trimethylpyrazine,CXC137 and CXC195 after cerebral ischemia were better than ligustrazine. | Hai-jun Gao Peng-fei Liu Pei-wen Li Zhuo-yan Huang Feng-bo Yu Ting Lei Yong Chen Ye Cheng Qing-chun Mu Hai-yan Huang | 2015 | Neural Regeneration Research2015，10，5： | 48 |
| 9 | Epalrestat protects against diabetic peripheral neuropathy by alleviating oxidative stress and inhibiting polyol pathway显示文摘Epalrestat is a noncompetitive and reversible aldose reductase inhibitor used for the treatment of diabetic neuropathy. This study assumed that epalrestat had a protective effect on diabetic peripheral nerve injury by suppressing the expression of aldose reductase in peripheral nerves of diabetes mellitus rats. The high-fat and high-carbohydrate model rats were established by intraperitoneal injection of streptozotocin. Peripheral neuropathy occurred in these rats after sustaining high blood glucose for 8 weeks. At 12 weeks after streptozotocin injection, rats were intragastrically administered epalrestat 100 mg/kg daily for 6 weeks. Transmission electron microscope revealed that the injuries to myelinated nerve fibers, non-myelinated nerve fibers and Schwann cells of rat sciatic nerves had reduced compared to rats without epalrestat administuation. Western blot assay and immunohistochemical results demonstrated that after intervention with epalrestat, the activities of antioxidant enzymes such as superoxide dismutase, catalase and glutathione peroxidase gradually increased, but aldose reductase protein expression gradually diminished. Results confirmed that epalrestat could protect against diabetic peripheral neuropathy by relieving oxidative stress and suppressing the polyol pathway. | Qing-rong Li Zhuo Wang Wei Zhou Shou-rui Fan Run Ma Li Xue Lu Yang Ya-shan Li Hong-li Tan Qi, ng-hua Shao Hong-ying Yang | 2016 | Neural Regeneration Research2016，11，2： | 42 |
| 10 | Puerarin protects rat brain against ischemia/reperfusion injury by suppressing autophagy via the AMPK-mT OR-ULK1 signaling pathway显示文摘Puerarin suppresses autophagy to alleviate cerebral ischemia/reperfusion injury, and accumulating evidence indicates that the AMPKm TOR signaling pathway regulates the activation of the autophagy pathway through the coordinated phosphorylation of ULK1. In this study, we investigated the mechanisms underlying the neuroprotective effect of puerarin and its role in modulating autophagy via the AMPK-m TOR-ULK1 signaling pathway in the rat middle cerebral artery occlusion model of cerebral ischemia/reperfusion injury. Rats were intraperitoneally injected with puerarin, 50 or 100 mg/kg, daily for 7 days. Then, 30 minutes after the final administration, rats were subjected to transient middle cerebral artery occlusion for 90 minutes. Then, after 24 hours of reperfusion, the Longa score and infarct volume were evaluated in each group. Autophagosome formation was observed by transmission electron microscopy. LC3, Beclin-1 p62, AMPK, m TOR and ULK1 protein expression levels were examined by immunofluorescence and western blot assay. Puerarin substantially reduced the Longa score and infarct volume, and it lessened autophagosome formation in the hippocampal CA1 area following cerebral ischemia/reperfusion injury in a dose-dependent manner. Pretreatment with puerarin(50 or 100 mg/kg) reduced Beclin-1 expression and the LC3-II/LC3-I ratio, as well as p-AMPK and p S317-ULK1 levels. In comparison, it increased p62 expression. Furthermore, puerarin at 100 mg/kg dramatically increased the levels of p-m TOR and p S757-ULK1 in the hippocampus on the ischemic side. Our findings suggest that puerarin alleviates autophagy by activating the APMK-m TOR-ULK1 signaling pathway. Thus, puerarin might have therapeutic potential for treating cerebral ischemia/reperfusion injury. | Jin-Feng Wang Zhi-Gang Mei Yang Fu Song-Bai Yang Shi-Zhong Zhang Wei-Feng Huang Li Xiong Hua-Jun Zhou Wei Tao Zhi-Tao Feng | 2018 | Neural Regeneration Research2018，13，6： | 45 |
| 11 | Mechanism underlying treatment of ischemic stroke using acupuncture:transmission and regulation显示文摘The inflammatory response after cerebral ischemia/reperfusion is an important cause of neurological damage and repair.After cerebral ischemia/reperfusion,microglia are activated,and a large number of circulating inflammatory cells infiltrate the affected area.This leads to the secretion of inflammatory mediators and an inflammatory cascade that eventually causes secondary brain damage,including neuron necrosis,blood-brain barrier destruction,cerebral edema,and an oxidative stress response.Activation of inflammatory signaling pathways plays a key role in the pathological process of ischemic stroke.Increasing evidence suggests that acupuncture can reduce the inflammatory response after cerebral ischemia/reperfusion and promote repair of the injured nervous system.Acupuncture can not only inhibit the activation and infiltration of inflammatory cells,but can also regulate the expression of inflammation-related cytokines,balance the effects of pro-inflammatory and anti-inflammatory factors,and interfere with inflammatory signaling pathways.Therefore,it is important to study the transmission and regulatory mechanism of inflammatory signaling pathways after acupuncture treatment for cerebral ischemia/reperfusion injury to provide a theoretical basis for clinical treatment of this type of injury using acupuncture.Our review summarizes the overall conditions of inflammatory cells,mediators,and pathways after cerebral ischemia/reperfusion,and discusses the possible synergistic intervention of acupuncture in the inflammatory signaling pathway network to provide a foundation to explore the multiple molecular mechanisms by which acupuncture promotes nerve function restoration. | Bing-Qian Cao Feng Tan Jie Zhan Peng-Hui Lai | 2021 | Neural Regeneration Research2021，16，5： | 43 |
| 12 | Electroacupuncture improves learning and memory functions in a rat cerebral ischemia/reperfusion injury model through PI3K/Akt signaling pathway activation显示文摘Electroacupuncture has been widely used to treat cognitive impairment after cerebral ischemia,but the underlying mechanism has not yet been fully elucidated.Studies have shown that autophagy plays an important role in the formation and development of cognitive impairment,and the phosphoinositide 3-kinase(PI3K)/Akt signaling pathway plays an important role in autophagy regulation.To investigate the role played by the PI3K/Akt signaling pathway in the electroacupuncture treatment of cerebral ischemia/reperfusion rat models,we first established a rat model of cerebral ischemia/reperfusion through the occlusion of the middle cerebral artery using the suture method.Starting at 2 hours after modeling,electroacupuncture was delivered at the Shenting(GV24)and Baihui(GV20)acupoints,with a dilatational wave(1-20 Hz frequency,2 mA intensity,6 V peak voltage),for 30 minutes/day over 8 consecutive days.Our results showed that electroacupuncture reduced the infarct volume in a rat model of cerebral ischemia/reperfusion injury,increased the mRNA expression levels of the PI3K/Akt signaling pathwayrelated factors Beclin-1,mammalian target of rapamycin(mTOR),and PI3K,increased the protein expression levels of phosphorylated Akt,Beclin-1,PI3K,and mTOR in the ischemic cerebral cortex,and simultaneously reduced p53 mRNA and protein expression levels.In the Morris water maze test,the latency to find the hidden platform was significantly shortened among rats subjected to electroacupuncture stimulation compared with rats without electroacupuncture stimulation.In the spatial probe test,the number of times that a rat crossed the target quadrant was increased in rats subjected to electroacupuncture stimulation compared with rats without electroacupuncture stimulation.Electroacupuncture stimulation applied to the Shenting(GV24)and Baihui(GV20)acupoints activated the PI3K/Akt signaling pathway and improved rat learning and memory impairment.This study was approved by the Animal Ethics Committee of the First Affiliated Hospital of Henan University of Traditional Chinese Medicine,China(approval No.8150150901)on March 10,2016. | Hui-Ling Wang Fei-Lai Liu Rui-Qing Li Ming-Yue Wan Jie-Ying Li Jing Shi Ming-Li Wu Jun-Hua Chen Wei-Juan Sun Hong-Xia Feng Wei Zhao Jin Huang Ren-Chao Liu Wen-Xue Hao Xiao-Dong Feng | 2021 | Neural Regeneration Research2021，16，6： | 48 |
| 13 | Puerarin partly counteracts the inflammatory response after cerebral ischemia/reperfusion via activating the cholinergic anti-inflammatory pathway显示文摘Puerarin,a major isoflavonoid derived from the Chinese medical herb radix puerariae(Gegen),has been reported to inhibit neuronal apoptosis and play an anti-inflammatory role in focal cerebra ischemia model rats.Recent findings regarding stroke pathophysiology have recognized that anti-inflammation is an important target for the treatment of ischemic stroke.The cholinergic anti-inflammatory pathway is a highly robust neural-immune mechanism for inflammation control This study was to investigate whether activating the cholinergic anti-inflammatory pathway can be involved in the mechanism of inhibiting the inflammatory response during puerarin-induced cerebra ischemia/reperfusion in rats.Results showed that puerarin pretreatment(intravenous injection)reduced the ischemic infarct volume,improved neurological deficit after cerebra ischemia/reperfusion and decreased the levels of interleukin-1β,interleukin-6 and tumor necrosis factor-αin brain tissue.Pretreatment with puerarin(intravenous injection)attenuated the inflammatory response in rats,which was accompanied by janus-activated kinase 2(JAK2)and signal transducers and activators of transcription 3(STAT3)activation and nuclear factor kappa B(NF-κB)inhibition.These observations were inhibited by the alpha7 nicotinic acetylcholine recepto(α7nAchR)antagonistα-bungarotoxin(α-BGT).In addition,puerarin pretreatment increased the expression ofα7nAchR mRNA in ischemic cerebral tissue.These data demonstrate that puerarin pretreatment strongly protects the brain against cerebral ischemia/reperfusion injury and inhibits the inflammatory response.Our results also indicated that the anti-inflammatory effect of puerarin may partly be mediated through the activation of the cholinergic anti-inflammatory pathway. | Xiaojie Liu Zhigang Mei Jingping Qian Yongbao Zeng Mingzhi Wang | 2013 | Neural Regeneration Research2013，8，34： | 39 |
| 14 | Deferoxamine promotes recovery of traumatic spinal cord injury by inhibiting ferroptosis显示文摘Ferroptosis is an iron-dependent novel cell death pathway. Deferoxamine, a ferroptosis inhibitor, has been reported to promote spinal cord injury repair. It has yet to be clarified whether ferroptosis inhibition represents the mechanism of action of Deferoxamine on spinal cord injury recovery. A rat model of Deferoxamine at thoracic 10 segment was established using a modified Allen's method. Ninety 8-week-old female Wistar rats were used. Rats in the Deferoxamine group were intraperitoneally injected with 100 mg/kg Deferoxamine 30 minutes before injury. Simultaneously, the Sham and Deferoxamine groups served as controls. Drug administration was conducted for 7 consecutive days. The results were as follows:(1) Electron microscopy revealed shrunken mitochondria in the spinal cord injury group.(2) The Basso, Beattie and Bresnahan locomotor rating score showed that recovery of the hindlimb was remarkably better in the Deferoxamine group than in the spinal cord injury group.(3) The iron concentration was lower in the Deferoxamine group than in the spinal cord injury group after injury.(4) Western blot assay revealed that, compared with the spinal cord injury group, GPX4, xCT, and glutathione expression was markedly increased in the Deferoxamine group.(5) Real-time polymerase chain reaction revealed that, compared with the Deferoxamine group, mRNA levels of ferroptosis-related genes Acyl-CoA synthetase family member 2(ACSF2) and iron-responsive element-binding protein 2(IREB2) were up-regulated in the Deferoxamine group.(6) Deferoxamine increased survival of neurons and inhibited gliosis. These findings confirm that Deferoxamine can repair spinal cord injury by inhibiting ferroptosis. Targeting ferroptosis is therefore a promising therapeutic approach for spinal cord injury. | Xue Yao Yan Zhang Jian Hao Hui-Quan Duan Chen-Xi Zhao Chao Sun Bo Li Bao-You Fan Xu Wang Wen-Xiang Li Xuan-Hao Fu Yong Hu Chang Liu Xiao-Hong Kong Shi-Qing Feng | 2019 | Neural Regeneration Research2019，14，3： | 35 |
| 15 | Inhibition of cerebral ischemia/reperfusion injuryinduced apoptosis:nicotiflorin and JAK2/STAT3 pathway显示文摘Nicotiflorin is a flavonoid extracted from Carthamus tinctorius.Previous studies have shown its cerebral protective effect,but the mechanism is undefined.In this study,we aimed to determine whether nicotiflorin protects against cerebral ischemia/reperfusion injury-induced apoptosis through the JAK2/STAT3 pathway.The cerebral ischemia/reperfusion injury model was established by middle cerebral artery occlusion/reperfusion.Nicotiflorin(10 mg/kg) was administered by tail vein injection.Cell apoptosis in the ischemic cerebral cortex was examined by hematoxylin-eosin staining and terminal deoxynucleotidyl transferase d UTP nick end labeling assay.Bcl-2 and Bax expression levels in ischemic cerebral cortex were examined by immunohistochemial staining.Additionally,p-JAK2,p-STAT3,Bcl-2,Bax,and caspase-3 levels in ischemic cerebral cortex were examined by western blot assay.Nicotiflorin altered the shape and structure of injured neurons,decreased the number of apoptotic cells,down-regulates expression of p-JAK2,p-STAT3,caspase-3,and Bax,decreased Bax immunoredactivity,and increased Bcl-2 protein expression and immunoreactivity.These results suggest that nicotiflorin protects against cerebral ischemia/reperfusion injury-induced apoptosis via the JAK2/STAT3 pathway. | Guang-qiang Hu Xi Du Yong-jie Li Xiao-qing Gao Bi-qiong Chen Lu Yu | 2017 | Neural Regeneration Research2017，12，1： | 40 |
| 16 | Low frequency repetitive transcranial magnetic stimulation improves motor dysfunction after cerebral infarction显示文摘Low frequency(≤ 1 Hz) repetitive transcranial magnetic stimulation(r TMS) can affect the excitability of the cerebral cortex and synaptic plasticity. Although this is a common method for clinical treatment of cerebral infarction, whether it promotes the recovery of motor function remains controversial. Twenty patients with cerebral infarction combined with hemiparalysis were equally and randomly divided into a low frequency r TMS group and a control group. The patients in the low frequency r TMS group were given 1-Hz r TMS to the contralateral primary motor cortex with a stimulus intensity of 90% motor threshold, 30 minutes/day. The patients in the control group were given sham stimulation. After 14 days of treatment, clinical function scores(National Institute of Health Stroke Scale, Barthel Index, and Fugl-Meyer Assessment) improved significantly in the low frequency r TMS group, and the effects were better than that in the control group. We conclude that low frequency(1 Hz) r TMS for 14 days can help improve motor function after cerebral infarction. | Zhi-yong Meng Wei-qun Song | 2017 | Neural Regeneration Research2017，12，4： | 40 |
| 17 | Relationship of nocturnal concentrations of melatonin, gamma-aminobutyric acid and total antioxidants in peripheral blood with insomnia after stroke: study protocol for a prospective non-randomized controlled trial显示文摘Melatonin and gamma-aminobutyric acid(GABA) have been shown to regulate sleep. The nocturnal concentrations of melatonin, GABA and total antioxidants may relate to insomnia in stroke patients. In this prospective single-center non-randomized controlled clinical trial performed in the China Rehabilitation Research Center, we analyzed the relationship of nocturnal concentrations of melatonin, GABA and total antioxidants with insomnia after stroke. Patients during rehabilitation of stroke were recruited and assigned to the insomnia group or non-insomnia group. Simultaneously, persons without stroke or insomnia served as normal controls. Each group contained 25 cases. The primary outcome was nocturnal concentrations of melatonin, GABA and total antioxidants in peripheral blood. The secondary outcomes were Pittsburgh Sleep Quality Index, Insomnia Severity Index, Epworth Sleepiness Scale, Fatigue Severity Scale, Morningness-Eveningness Questionnaire(Chinese version), and National Institute of Health Stroke Scale. The relationship of nocturnal concentrations of melatonin, GABA and total antioxidants with insomnia after stroke was analyzed and showed that they were lower in the insomnia group than in the non-insomnia group. The severity of stroke was higher in the insomnia group than in the non-insomnia group. Correlation analysis demonstrated that the nocturnal concentrations of melatonin and GABA were associated with insomnia after stroke. This trial was registered at Clinical Trials.gov, identifier: NCT03202121. | Wei Zhang Fang Li Tong Zhang | 2017 | Neural Regeneration Research2017，12，8： | 39 |
| 18 | Acupuncture and neuroregeneration in ischemic stroke显示文摘Acupuncture is potentially beneficial for post-stroke rehabilitation and is considered a promising preventive strategy for stroke.Electroacupuncture pretreatment or treatment after ischemic stroke by using appropriate electroacupuncture parameters generates neuroprotective and neuroregenerative effects that increase cerebral blood flow,regulate oxidative stress,attenuate glutamate excitotoxicity,maintain bloodbrain barrier integrity,inhibit apoptosis,increase growth factor production,and induce cerebral ischemic tolerance. | Qwang-Yuen Chang Yi-Wen Lin Ching-Liang Hsieh | 2018 | Neural Regeneration Research2018，13，4： | 38 |
| 19 | Autophagy: novel insights into therapeutic target of electroacupuncture against cerebral ischemia/reperfusion injury显示文摘Electroacupuncture is known as an effective adjuvant therapy in ischemic cerebrovascular disease. However, its underlying mechanisms remain unclear. Studies suggest that autophagy, which is essential for cell survival and cell death, is involved in cerebral ischemia reperfusion injury and might be modulate by electroacupuncture therapy in key ways. This paper aims to provide novel insights into a therapeutic target of electroacupuncture against cerebral ischemia/reperfusion injury from the perspective of autophagy. Here we review recent studies on electroacupuncture regulation of autophagy-related markers such as UNC-51-like kinase-1 complex, Beclin1, microtubule-associated protein-1 light chain 3, p62, and autophagosomes for treating cerebral ischemia/reperfusion injury. The results of these studies show that electroacupuncture may affect the initiation of autophagy, vesicle nucleation, expansion and maturation of autophagosomes, as well as fusion and degradation of autophagolysosomes. Moreover, studies indicate that electroacupuncture probably modulates autophagy by activating the mammalian target of the rapamycin signaling pathway.This review thus indicates that autophagy is a therapeutic target of electroacupuncture treatment against ischemic cerebrovascular diseases. | Ya-Guang Huang Wei Tao Song-Bai Yang Jin-Feng Wang Zhi-Gang Mei Zhi-Tao Feng | 2019 | Neural Regeneration Research2019，14，6： | 39 |
| 20 | Mechanism of delayed encephalopathy after acute carbon monoxide poisoning显示文摘Many hypotheses exist regarding the mechanism underlying delayed encephalopathy after acute carbon monoxide poisoning(DEACMP),including the inflammation and immune-mediated damage hypothesis and the cellular apoptosis and direct neuronal toxicity hypothesis;however,no existing hypothesis provides a satisfactory explanation for the complex clinical processes observed in DEACMP.Leucine-rich repeat and immunoglobulin-like domain-containing protein-1(LINGO-1)activates the Ras homolog gene family member A(Rho A)/Rho-associated coiled-coil containing protein kinase 2(ROCK2)signaling pathway,which negatively regulates oligodendrocyte myelination,axonal growth,and neuronal survival,causing myelin damage and participating in the pathophysiological processes associated with many central nervous system diseases.However,whether LINGO-1 is involved in DEACMP remains unclear.A DEACMP model was established in rats by allowing them to inhale 1000 ppm carbon monoxide gas for 40 minutes,followed by 3000 ppm carbon monoxide gas for an additional 20 minutes.The results showed that compared with control rats,DEACMP rats showed significantly increased water maze latency and increased protein and m RNA expression levels of LINGO-1,Rho A,and ROCK2 in the brain.Compared with normal rats,significant increases in injured neurons in the hippocampus and myelin sheath damage in the lateral geniculate body were observed in DEACMP rats.From days 1 to 21 after DEACMP,the intraperitoneal injection of retinoic acid(10 mg/kg),which can inhibit LINGO-1 expression,was able to improve the above changes observed in the DEACMP model.Therefore,the overexpression of LINGO-1 appeared to increase following carbon monoxide poisoning,activating the Rho A/ROCK2 signaling pathway,which may be an important pathophysiological mechanism underlying DEACMP.This study was reviewed and approved by the Medical Ethics Committee of Xiangya Hospital of Central South Hospital(approval No.201612684)on December 26,2016. | Yan-Qing Huang Zheng-Rong Peng Fang-Ling Huang A-Li Yang | 2020 | Neural Regeneration Research2020，15，12： | 35 |
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