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Nanomolar concentration of alpha-synuclein enhances dopaminergic neuronal survival via Akt pathway

Neural Regeneration Research 2013年第35期8卷 3269-3274页

作者： Ji-Young Kim Beom Seok Jeon Han-Joon Kim Tae-Beom Ahn Department of Neurology Inje University Seoul Paik Hospital Department of Neurology College of Medicine Seoul National University Hospital Department of Neurology Kyung Hee University Medical Center

Although alpha-synuclein is generally thought to have a pathological role in Parkinson＇s disease, accumulative evidence exists that alpha-synuclein has a neuroprotective effect. The aim of this study was to evaluate the effect of extracellular alpha-synuclein on dopaminergic cell survival. We assessed cell viability using the 3-（4,5-dimethyt-thiazol-2-yt）-2,5-diphenyltertazolium bromide （MTT） assay both in undifferentiated SH-SY5Y （SHSY） cells and neuronally-differentiated SH-SY5Y （ndSHSY） cells after 24 hour treatment with monomeric alpha-synuclein at various concentrations （0 [control], 50, 100 nmol/L, 1 IJmol/L）. To determine whether cell viability assessed by MTT assay was affected by cell proliferation, 5-bromo-2＇-deoxyuridine （BrdU） incorporation assay was per- formed. Level of both Akt and phosphorylated Akt was measured using western blot method in ndSHSY cells with or without 24 hour alpha-synuclein treatment. Cell viability was increased in ndSHSY cells at the nanomolar concentration of alpha-synuclein, but not in SHSY cells. Proportion of BrdU-positive ndSHSY cells was decreased in alpha-synuclein-treated group compared with control group. Level of phosphorylated Akt in alpha-synuclein-treated group was higher compared with the control group. Our study shows that extracellular alpha-synuclein at nanomolar concentra- tion benefits dopaminergic cell survival via Akt pathway.

关键词： neural regeneration alpha-synuclein neuronal survival nanomolar extracellular phosphorylatedAkt SH-SY5Y cell neuronal differentiation proliferation dopaminergic 5-bromo-2'-deoxyuridine grants-supported paper neuroregeneration

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RhoA as a target to promote neuronal survival and axon regeneration

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Neural Regeneration Research 2017年第4期12卷 525-528页

作者： Jianli Hu Michael E. Seizer Shriners Hospitals for Children Pediatric Research Center (Center for Neural Repair and Rehabilitation) Lewis Katz School of Medicine at Temple University Philadelphia PA USA Department of Neurology Lewis Katz School of Medicine at Temple University Philadelphia PA USA

Paralysis following spinal cord injury （SCI） is due to failure of axonal regeneration. It is believed that the capacities of neurons to regrow their axons are due partly to their intrinsic characteristics, which in turn are greatly influenced by several types of inhibitory molecules that are present, or even increased in the extracellular environment of the injured spinal cord. Many of these inhibitory molecules have been studied extensively in recent years. It has been suggested that the small GTPase RhoA is an intracellular convergence point for signaling by these extracellular inhibitory molecules, but due to the complexity of the central nervous system （CNS） in mammals, and the limitation of pharmacological tools, the specific roles of RhoA are unclear. By exploiting the anatomical and technical advantages of the lamprey CNS, we recently demonstrated that RhoA knockdown promotes true axon regeneration through the lesion site after SCI. In addition, we found that RhoA knockdown protects the large, identified reticulospinal neurons from apoptosis after their axons were axotomized in spinal cord. Therefore, manipulation of the RhoA signaling pathway may be an important approach in the development of treatments that are both neuroprotective and axon regeneration-promoting, to enhance functional recovery after SCI.

关键词： RhoA spinal cord injury neuronal survival apoptosis axon regeneration morpholino C3 transferase

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Trans-Cinnamaldehyde Inhibits Microglial Activation and Improves neuronal survival against Neuroinflammationin vitro and in vivo

Trans-Cinnamaldehyde Inhibits Microglial Activation and Impr...

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中国生理学会第24届全国会员代表大会暨生理学学术大会

作者： Liqing Zhang Zhangang Zhang Zhongping Wu Ying Xu Department of Physiology Shanghai University of Traditional Chinese Medicine Teaching & Research Department of Clinical and Classic Medicine Shanghai University of Traditional Chinese Medicine

Background:Microglial activation contributes to neuroinflammation and neuronal damages in neurodegenerative disorders including Alzheimer’s and Parkinson’s *** has been suggested that neurodegenerative disorders may be improved if neuroinflammation can be ***-cinnamaldehyde（TCA）isolated from the stem bark of Cinnamomum cassia possess potent anti-inflammatory capability,we thus tested whether TCA presents neuroprotective effecton prefrontal cortex and hippocampal CA1by inhibiting neuroinflammatory responses in vitro and in ***:To determine the molecular mechanism behind TCA-mediated neuroprotective effect,we assessed the effect of TCA on LPS-induced pro-inflammatory responses in BV2 microglia *** LPS potently induced the production of nitric oxide（NO）,tumor necrosis factor alpha（TNF-α）and interleukin-1 beta（IL-1β）,their production was significantly inhibited by treatment of *** the aid of microglial and neuron co-culture system,we showed that TCA greatly reduced lipopolysaccharide（LPS）-elicited neuronal cell ***,TCA also markedly attenuated microglial activation and increased neuronal density in prefrontal cortexand hippocampal CA1 with LPS-induced neuroinflammation in vivo ***:Our results suggest that TCA has the potential of being used as a chemoprevention agent against neuroinflammation in neurodegenerative disorders.

关键词： Trans-cinnamaldehyde Neuroinflammation Neurodegenerative disorders Microglial activation neuronal survival

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Role of Tyro-3 receptors playing at neuronal survival in central nervous system

Role of Tyro-3 receptors playing at neuronal survival in cen...

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中国神经科学学会第四次会员代表大会暨第七届全国学术会议

作者： Yan ZHENG,Qing-Xian LU,Xiao-Min WANG~* Key laboratory of Neurodegenerative Diseases of the Ministry of Education,Capital Medical University,Beijing 100069,China

Tyro-3 receptors are identified as a novel and distinct receptor PTK subgroup including Tyro-3,Mer and Axl. There are two ligands for these receptors--Protein S and growth arrest specific gene6 product Gas6 exclusively expressed in cells of the *** have found that Tyro-3 receptors especially Tyro-3 and Axl expressed in cortex and hippocampus of CNS *** examine whether Tyro-3 receptors can affect the neuronal survival in these areas in *** studied the pathologic changes in brain of triple genes encoding Tyro-3,Axl and Mer-knockout mice at first and we found the evident neuronal degeneration and loss of neurons in cortex and hippocampus in triple mutant mice compared to that of normal *** immunoreactivity positive neurons and TUNEL staining positive neurons were also observed in the two brain *** functions of Tyro-3 receptors and their ligands in the nervous system are not well understood,dispite their predominant in the *** detected that recombinant mouse Gas6 oligomer (10μmol/L) and serum deprivation,respectively in vitro,indicating that Gas6 have neurotrophic roles in the nervous *** neuroprotective effects exhibited by Gas6 was through activation of phosphatidylinositol3-OH kinase (PI3K)/Akt signaling pathway in neurons since pretreatment of inhibitor for PI3K-LY294002 could block the effects. Moreover,western blotting assay revealed that Gas6 activated the Akt which is the downstream target of receptor tyrosine kinases-PI3K system in time-dependent manner in hippocampal neurons and PC 12 cells differentiated by ***, Tyro-3 receptors are necessary in mediating the neuroprotective effects showed by *** deficiency in central nervous system could result in disfunction of neuronal survival.

关键词： Tyro-3 receptors neurotrophic effects neuronal survival central nervous system

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Inhibition of LncRNA Vof-16 expression promotes nerve regeneration and functional recovery after spinal cord injury

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Neural Regeneration Research 2022年第1期17卷 217-227页

作者： Xiao-Min Zhang Li-Ni Zeng Wan-Yong Yang Lu Ding Kang-Zhen Chen Wen-Jin Fu Si-Quan Zeng Yin-Ru Liang Gan-Hai Chen Hong-Fu Wu Key Laboratory of Stem Cell and Regenerative Tissue Engineering Guangdong Medical UniversityDongguanGuangdong ProvinceChina Biology Research Group Guangzheng Experimental SchoolHuizhouGuangdong ProvinceChina Geriatric Medicine Center Dongguan Waterfront Zone Central HospitalDongguanGuangdong ProvinceChina Scientific Research Center the Seventh Affiliated HospitalSun Yat-sen UniversityShenzhenGuangdong ProvinceChina Clinical Laboratory Affiliated Houjie HospitalGuangdong Medical UniversityDongguanGuangdong ProvinceChina Department of Intensive Care Unit Affiliated Houjie HospitalGuangdong Medical UniversityDongguanGuangdong ProvinceChina

Our previous RNA sequencing study showed that the long non-coding RNA ischemia-related factor Vof-16(lncRNA Vof-16)was upregulated after spinal cord injury,but its precise role in spinal cord injury remains *** predictions have indicated that lncRNA Vof-16 may participate in the pathophysiological processes of inflammation and ***12 cells were transfected with a pHBLV-U6-MCS-CMV-ZsGreen-PGK-PURO vector to express an lncRNA Vof-16 knockdown lentivirus and a pHLV-CMVIE-ZsGree-Puro vector to express an lncRNA Vof-16 overexpression *** overexpression of lncRNA Vof-16 inhibited PC12 cell survival,proliferation,migration,and neurite extension,whereas lncRNA Vof-16 knockdown lentiviral vector resulted in the opposite effects in PC12 *** blot assay results showed that the overexpression of lncRNA Vof-16 increased the protein expression levels of interleukin 6,tumor necrosis factor-α,and Caspase-3 and decreased Bcl-2 expression levels in PC12 ***,we established rat models of spinal cord injury using the complete transection at *** cord injury model rats were injected with the lncRNA Vof-16 knockdown or overexpression lentiviral vectors immediately after *** 7 days after spinal cord injury,rats treated with lncRNA Vof-16 knockdown displayed increased neuronal survival and enhanced axonal *** 8 weeks after spinal cord injury,rats treated with the lncRNA Vof-16 knockdown lentiviral vector displayed improved neurological function in the hind ***,lncRNA Vof-16 knockdown injection increased Bcl-2 expression and decreased tumor necrosis factor-αand Caspase-3 expression in treated *** treated with the lncRNA Vof-16 overexpression lentiviral vector displayed opposite *** findings suggested that lncRNA Vof-16 is associated with the regulation of inflammation and *** inhibition of lncRNA Vof-16 may be useful for promoting nerve regeneration and functional recovery a

关键词： apoptosis functional recovery inflammation long non-coding RNA ischemia related factor Vof-16 nerve regeneration nerve repair neurite extension neuronal survival proliferation spinal cord injury

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Neurotrophic fragments as therapeutic alternatives to ameliorate brain aging

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Neural Regeneration Research 2023年第1期18卷 51-56页

作者： Itzel Ortiz Flores Samuel Treviño Alfonso Díaz Department of Health Sciences School of MedicineUniversity of the Americas PueblaPueblaMexico Faculty of Chemical Sciences Benemerita Autonomous University of PueblaPueblaMexico

Aging is a global phenomenon and a complex biological process of all living beings that introduces various *** this physiological process,the brain is the most affected organ due to changes in its structural and chemical functions,such as changes in plasticity and decrease in the number,diameter,length,and branching of dendrites and dendritic ***,it presents a great reduction in volume resulting from the contraction of the gray ***,aging can affect not only cognitive functions,including learning and memory,but also the quality of life of older *** a result of the phenomena,various molecules with notable neuroprotective capacity have been proposed,which provide a therapeutic alternative for people under conditions of aging or some neurodegenerative *** is important to indicate that in recent years the use of molecules with neurotrophic activity has shown interesting results when evaluated in in vivo *** review aims to describe the neurotrophic potential of molecules such as resveratrol(3,5,4′-trihydroxystilbene),neurotrophins(brain-derived neurotrophic factor),and neurotrophic-type compounds such as the terminal carboxyl domain of the heavy chain of tetanus toxin,cerebrolysin,neuropeptide-12,and *** of these molecules have been evaluated by our research *** suggest that these molecules exert an important therapeutic potential,restoring brain function in aging conditions or models of neurodegenerative ***,our interest is in describing the current scientific evidence that supports the therapeutic potential of these molecules with active neurotrophic.

关键词： Alzheimer’s disease brain cerebral cortex cognitive function dendritic spines HC-TeTx hippocampus neurodegeneration neuronal survival neurotrophins

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Dose-dependent and combined effects of N-methyl-D-aspartate receptor antagonist MK-801 and nitric oxide synthase inhibitor nitro-L-arginine on the survival of retinal ganglion cells in adult hamsters

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Neural Regeneration Research 2012年第10期7卷 725-730页

作者： Yaoyu Li An＇an Yang Tingting Zhu Zhao Liu Siwei You Kwok-Fai So Department of Ophthalmology General Hospital of Beijing Military Region Beijing 100700 China Institute of Neurosciences the Fourth Military Medical University Xi＇an 710032 Shaanxi Province China Department of Anatomy Li Ka Shing Faculty of Medicine The University of Hong Kong Hong Kong Special Administrative Region China

This study investigated the effects of daily intraperitoneal injections of N-methyl-D-aspartate receptor antagonist MK-801 and nitric oxide synthase inhibitor nitro-L-arginine （L-NA） on the survival of retinal ganglion cells （RGCs） at 1 and 2 weeks after unilateral optic nerve transection in adult hamsters. The left optic nerves of all animals were transected intraorbitally 1 mm from the optic disc and RGCs were retrogradely labeled with Fluorogold before they received different daily dosages of single MK-801 or L-NA as well as daily combinational treatments of these two chemicals. All experimental and control animals survived for 1 or 2 weeks after optic nerve transection. Our results revealed that the mean numbers of surviving RGCs increased and then decreased when the dosage of MK-801 （1.0, 3.0 and 4.5 mg/kg） and L-NA （1.5, 3.0, 4.5 and 6.0 mg/kg） increased at both 1 and 2 weeks survival time points. Daily combinational use of 1.0 mg/kg MK-801 and 1.5 mg/kg L-NA lead to a highest RGC number that was even higher than the sum of the RGC numbers in 1.0 mg/kg MK-801 and 1.5 mg/kg L-NA subgroups at 2 weeks. These findings indicated that both MK-801 and L-NA can protect axotomized RGCs in a dose-dependent manner and combinational treatment of these chemicals possesses a potentiative and protective effect.

关键词： retinal ganglion cells optic nerve transection N-methyl-D-aspartate receptor nitric oxide synthase neuronal survival hamster

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Micro RNA-124 slows down the progression of Huntington's disease by promoting neurogenesis in the striatum

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Neural Regeneration Research 2015年第5期10卷 786-791页

作者： Tian Liu Wooseok Im Inhee Mook-Jung Manho Kim Department of Biomedical Sciences Seoul National University College of Medicine Department of Neurology Biomedical Research InstituteSeoul National University Hospital Department of Biochemistry Seoul National University College of Medicine Protein Metabolism Medical Research Center College of MedicineSeoul National University

MicroRNA-124 contributes to neurogenesis through regulating its targets, but its expression both in the brain of Huntington＇s disease mouse models and patients is decreased. However, the effects of microRNA-124 on the progression of Huntington＇s disease have not been reported. Results from this study showed that microRNA-124 increased the latency to fall for each R6/2 Hunting- ton＇s disease transgenic mouse in the rotarod test. 5-Bromo-2＇-deoxyuridine （BrdU） staining of the striatum shows an increase in neurogenesis. In addition, brain-derived neurotrophic factor and peroxisome proliferator-activated receptor gamma coactivator 1-alpha protein levels in the striatum were increased and SRY-related HMG box transcription factor 9 protein level was de- creased. These findings suggest that microRNA-124 slows down the progression of Huntington＇s disease possibly through its important role in neuronal differentiation and survival.

关键词： nerve regeneration microRNA-124 neurogenesis neuronal survival Huntington'sdisease SRY-related HMG box transcription factor 9 brain-derived neurotrophic factor peroxisomeproliferator-activated receptor gamma coactivator 1-alpha mutant huntingtin

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Effect of Interleukin-1Beta (IL-1β) on the Cortical Neurons survival and Neurites Outgrowth

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Advances in Bioscience and Biotechnology 2016年第1期7卷 28-37页

作者： Ebtesam M. Abd-El-Basset Department of Anatomy Faculty of Medicine Kuwait University Kuwait city Kuwait

Insults to the brain are known to cause a myriad of downstream effects, including the release of cytokines by astrocytes and resultant reactive gliosis. The author has examined effect of cytokine IL-1β on the survival of cortical neurons using mouse astrocyte-neuron co-culture. Five groups were used. These were neurons alone (Group 1), neurons with added IL-1β (Group 2), neurons co-cultured with astrocytes (Group 3), neurons co-cultured with astrocytes that was pre-treated with IL-1β before co-culture (Group 4) and neurons co-cultured with astrocytes and IL-1β added (post-treated) (Group 5). In Group 1 only a few neurons grew and survived only for 5-6 days. In Group 2, it was observed that more neurons survived up to 11 days. Moreover, in Group 3, more neurons grew and survived up to 16-18 days. They had large cell bodies and many long neurites that formed anastomosing networks. In Group 4, few neurons survived up to 13 days, whereas in Group 5, the growth of neurons were affected but to a much lesser extent than Group 4 and survived up to 15 days. In addition, it was found that IL-1β stimulated the expression of glial fibrillary acidic protein (GFAP) by astrocytes. This study indicates that IL-1β affects the survival of cortical neurons and modulates the astrocytic support to neuronal survival and neurites outgrowth by acting directly on the astrocytes.

关键词： Astrocytes IL-1β Cell Culture neuronal survival Cytokines Gliosis

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Combined effect of brain-derived neurotrophic factor and LINGO-1 fusion protein on long-term survival of retinal ganglion cells in chronic glaucoma

Combined effect of brain-derived neurotrophic factor and LIN...

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中国神经科学学会第四次会员代表大会暨第八届全国学术会议

作者： Henry K.Yip Kwok-Fai SO Department of Anatomy Li Ka Shing Faculty of MedicineThe University of Hong Kong The State Key Laboratory of Brain and Cognitive sciences The University of Hong Kong Research Centre of Heart BrainHormone and Healthy AgingThe University of Hong Kong

＜正＞Glaucoma is a progressive neuropathy characterized by loss of vision as a result of retinal ganglion cell（RGC） *** are no effective neuroprotectants to treat this ***-derived neurotrophic factor（BDNF） is well known to transiently delay RGC death in the ocular hypertentive *** central nervous system-specific leucine-rich repeat protein LINGO-1 contributes to the negative regulation to some trophic *** thereby examined whether BDNF combined with LINGO-1 antagonists can promote long-term RGC survival after ocular *** this study, intraocular pressure was elevated in adult rats using an argon laser to photocoagulate the episcleral and limbal veins. BDNF alone shows slight neuroprotection to RGCs after a long-term progress of 4 weeks following the induction of ocular ***,combination of BDNF and LINGO-1-Fc prevents RGC death in the same *** further identified that（1） LINGO-1 was co-expressed with BDNF receptor,TrkB in the RGCs,and（2） BDNF combined with LINGO- 1-Fc activated more TrkB in the injured retina compared to BDNF *** results indicate that the combination of BDNF with LINGO-1 antagonist can provide long-term protection for RGCs in a chronic ocular hypertension *** may be the predominant mediator of this neuroprotection.

关键词： ocular hypertension neural cells neuronal survival neurotrophic factors TrkB

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