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神经炎症与抑郁症相关的研究进展 预览
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作者 杨可心 《世界最新医学信息文摘(电子版)》 2019年第24期32-33,41共3页
抑郁症是一种常见的、损害严重的、经常复发的精神障碍,近年来人群中出现的不明原因的患病率逐渐上升。关于抑郁症的发病机制存在多种假设,这些假设尚未完全得到证实。最新的研究发现神经炎症与抑郁症的发生有关,NLRP3炎症小体、TNF-α... 抑郁症是一种常见的、损害严重的、经常复发的精神障碍,近年来人群中出现的不明原因的患病率逐渐上升。关于抑郁症的发病机制存在多种假设,这些假设尚未完全得到证实。最新的研究发现神经炎症与抑郁症的发生有关,NLRP3炎症小体、TNF-α细胞因子、星形胶质细胞与小胶质细胞均参与其中,为抑郁症的治疗提供了可能靶点。本文就神经炎症与抑郁症相关的研究进展进行分析。 展开更多
关键词 神经炎症 抑郁症 细胞因子 星形胶质细胞 小胶质细胞
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Extract of Fructus Schisandrae chinensis Inhibits Neuroinflammation Mediator Production from Microglia via NF-κB and MAPK Pathways
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作者 SONG Fang-jiao ZENG Ke-wu +4 位作者 CHEN Jin-feng LI Yuan SONG Xiao-min TU Peng-fei WANG Xue-mei 《中国结合医学杂志:英文版》 SCIE CAS CSCD 2019年第2期131-138,共8页
Objective: To investigate the anti-neuroinflammation effect of extract of Fructus Schisandrae chinensis(EFSC) on lipopolysaccharide(LPS)-induced BV-2 cells and the possible involved mechanisms. Methods: Primary cortic... Objective: To investigate the anti-neuroinflammation effect of extract of Fructus Schisandrae chinensis(EFSC) on lipopolysaccharide(LPS)-induced BV-2 cells and the possible involved mechanisms. Methods: Primary cortical neurons were isolated from embryonic(E17-18) cortices of Institute of Cancer Research(ICR) mouse fetuses. Primary microglia and astroglia were isolated from the frontal cortices of newborn ICR mouse. Different cells were cultured in specific culture medium. Cells were divided into 5 groups: control group, LPS group(treated with 1 μg/mL LPS only) and EFSC groups(treated with 1 μg/mL LPS and 100, 200 or 400 mg/mL EFSC, respectively). The effect of EFSC on cells viability was tested by methylthiazolyldiphenyltetrazolium bromide(MTT) colorimetric assay. EFSC-mediated inhibition of LPS-induced production of pro-inflammatory mediators, such as nitrite oxide(NO) and interleukin-6(IL-6) were quantified and neuron-protection effect against microglia-mediated inflammation injury was tested by hoechst 33258 apoptosis assay and crystal violet staining assay. The expression of pro-inflammatory marker proteins was evaluated by Western blot analysis or immunofluorescence. Results: EFSC(200 and 400 mg/mL) reduced NO, IL-6, inducible nitric oxide synthase(iN OS) and cyclooxygenase 2(COX-2) expression in LPS-induced BV-2 cel s(P<0.01 or P<0.05). EFSC(200 and 400 mg/mL) reduced the expression of NO in LPS-induced primary microglia and astroglia(P<0.01). In addition, EFSC al eviated cel apoptosis and inflammation injury in neurons exposed to microglia-conditioned medium(P<0.01). The mechanistic studies indicated EFSC could suppress nuclear factor(NF)-κB phosphorylation and its nuclear translocation(P<0.01). The anti-inflammatory effect of EFSC occurred through suppressed activation of mitogen-activated protein kinase(MAPK) pathway(P<0.01 or P<0.05). Conclusion: EFSC acted as an anti-inflammatory agent in LPS-induced glia cel s. These effects might be realized through blocking of NF-κB activity and inhibition of M 展开更多
关键词 NEUROINFLAMMATION MICROGLIA Fructus Schisandrae CHINENSIS nuclear factor-κB mitogen- activated protein KINASE
大气细颗粒物通过嗅球途径导致阿尔茨海默病的机制研究进展 预览
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作者 王昊 江杉 +3 位作者 龚杨明 刘燕 华丽 邓晓蓓 《上海交通大学学报:医学版》 CAS CSCD 北大核心 2019年第6期666-670,共5页
随着人们生活质量的提高,居民的寿命得到了普遍延长,老年痴呆发病的人数也不断增加。流行病学和动物实验研究均发现,大气颗粒物与阿尔茨海默病(Alzheimer′s disease,AD)的发生相关。该文综述了大气的细颗粒物通过嗅球途径进入大脑引起... 随着人们生活质量的提高,居民的寿命得到了普遍延长,老年痴呆发病的人数也不断增加。流行病学和动物实验研究均发现,大气颗粒物与阿尔茨海默病(Alzheimer′s disease,AD)的发生相关。该文综述了大气的细颗粒物通过嗅球途径进入大脑引起与AD相关的氧化应激损伤和神经炎症的机制。 展开更多
关键词 细颗粒物 阿尔茨海默病 嗅球 神经炎症 氧化应激
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Atsttrin reduces lipopolysaccharide-induced neuroinflammation by inhibiting the nuclear factor kappa B signaling pathway 预览
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作者 Lian Liu Yuan Qu +7 位作者 Yi Liu Hua Zhao He-Cheng Ma Ahmed Fayyaz Noor Chang-Jiao Ji Lin Nie Meng Si Lei Cheng 《中国神经再生研究:英文版》 SCIE CAS CSCD 2019年第11期1994-2002,共9页
Progranulin is closely related to neuronal survival in a neuroinflammatory mouse model and attenuates inflammatory reactions. Atsttrin is an engineered protein composed of three progranulin fragments and has been show... Progranulin is closely related to neuronal survival in a neuroinflammatory mouse model and attenuates inflammatory reactions. Atsttrin is an engineered protein composed of three progranulin fragments and has been shown to have an effect similar to that of progranulin. Atsttrin has anti-inflammatory actions in multiple arthritis mouse models, and it protects against further arthritis development. However, whether Atsttrin has a role in neuroinflammation remains to be elucidated. In this study, we produced a neuroinflammatory mouse model by intracerebroventricular injection of 1 μL lipopolysaccharide(10 μg/μL). Atsttrin(2.5 mg/kg) was administered via intraperitoneal injection every 3 days over a period of 7 days before intracerebroventricular injection of 1 μL lipopolysaccharide(10 μg/μL). In addition, astrocyte cultures were treated with 0, 100 or 300 ng/mL lipopolysaccharide, with 200 ng/mL Atsttrin simultaneously. Immunohistochemistry, enzyme-linked immunosorbent assay and real-time reverse transcription-polymerase chain reaction were performed to examine the protein and mRNA levels of inflammatory mediators and to assess activation of the nuclear factor kappa B signaling pathway. Progranulin expression in the brain of wild-type mice and in astrocyte cultures was increased after lipopolysaccharide administration. The protein and mRNA expression levels of tumor necrosis factor-α, interleukin-1β and inducible nitric oxide synthase were increased in the brain of progranulin knockout mice after lipopolysaccharide administration. Atsttrin treatment reduced the lipopolysaccharide-induced increase in the protein and mRNA levels of tumor necrosis factor-α, interleukin-1β, matrix metalloproteinase-3 and inducible nitric oxide synthase in the brain of progranulin knockout mice. Atsttrin also reduced the expression of cyclooxygenase-2, inducible nitric oxide synthase and matrix metalloproteinase 3 mRNA in lipopolysaccharide-treated astrocytes in vitro, and decreased the concentration of tumor necrosis factor α 展开更多
关键词 nerve REGENERATION progranulin Atsttrin NEUROINFLAMMATION inflammatory cytokines LIPOPOLYSACCHARIDE INTRACEREBROVENTRICULAR injection ASTROCYTE nuclear factor kappa B signaling pathway progranulin knockout mouse CEREBROSPINAL fluid neural REGENERATION
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帕金森病患者尸检迷走神经病理和肠道神经炎症分析
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作者 杨兆菲 孙雷 +3 位作者 寇大庆 李天白 孙志刚 乐卫东 《中华神经科杂志》 CAS CSCD 北大核心 2019年第5期387-393,共7页
目的探讨外周神经系统的神经炎性和病理改变在帕金森病发病中的作用。方法对1例帕金森病患者的捐献遗体的结状神经节(内含迷走神经)和肠道进行了免疫组织化学染色,观察迷走神经和肠道神经系统的神经炎性反应和不同部位的形态学改变。结... 目的探讨外周神经系统的神经炎性和病理改变在帕金森病发病中的作用。方法对1例帕金森病患者的捐献遗体的结状神经节(内含迷走神经)和肠道进行了免疫组织化学染色,观察迷走神经和肠道神经系统的神经炎性反应和不同部位的形态学改变。结果免疫组织化学染色显示,胶质细胞典型标志物神经胶质纤维酸性蛋白和小胶质细胞/巨噬细胞特异性蛋白离子钙结合接头分子1在迷走神经和肠道黏膜内细胞表达和分布不同。细胞炎性因子肿瘤坏死因子α与诱导型一氧化氮合酶在帕金森病尸检者肠道黏膜和肌间神经丛均表达。肌间神经丛存在较强的炎性反应,呈弥散样分布于肌间。结论迷走神经卫星胶质细胞和肠道炎性反应在帕金森病病因中可能起一定作用。 展开更多
关键词 帕金森病 神经炎症反应 肠道胶质细胞 迷走神经
Potential preventive disease-modifying pharmacological strategies to delay late onset Alzheimer’s disease 预览
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作者 Miren Ettcheto Oriol Busquets Antoni Camins 《中国神经再生研究:英文版》 SCIE CAS CSCD 2019年第10期1721-1725,共5页
Alzheimer’s disease(AD)is a progressive neurodegenerative disease that was histopathologically characterized in the brain by the presence of extracellular senile plaques made of amyloid β peptides and intracellular ... Alzheimer’s disease(AD)is a progressive neurodegenerative disease that was histopathologically characterized in the brain by the presence of extracellular senile plaques made of amyloid β peptides and intracellular neurofibrillary tangles composed of hyperphosphorylated Tau protein.Over the years,AD has been classified in two subgroups:early onset or familial AD and late onset or sporadic AD.On the one hand,familial AD has been described to be the result of genetic mutations that cause,in some cases,for the overproduction of amyloid β.On the other,the cause of late onset or sporadic AD is still unclear even though several hypotheses have been proposed to explain the process of severe and progressive memory and cognitive loss.In the present review,some of the current hypotheses that try to explain the origin of late onset or sporadic AD have been summarized.Also,their potential implication in the development of new drugs for the presymptomatic treatment of late onset or sporadic AD has been considered. 展开更多
关键词 Alzheimer's DISEASE BETA-SECRETASE NEUROINFLAMMATION Tau amyloid N-METHYL-D-ASPARTATE glutamate
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Resveratrol reduces brain injury after subarachnoid hemorrhage by inhibiting oxidative stress and endoplasmic reticulum stress 预览
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作者 Yun-Kai Xie Xin Zhou +5 位作者 Hong-Tao Yuan Jie Qiu Dan-Qing Xin Xi-Li Chu Da-Chuan Wang Zhen Wang 《中国神经再生研究:英文版》 SCIE CAS CSCD 2019年第10期1734-1742,共9页
Previous studies have shown that resveratrol,a bioactive substance found in many plants,can reduce early brain injury after subarachnoid hemorrhage,but how it acts is still unclear.This study explored the mechanism us... Previous studies have shown that resveratrol,a bioactive substance found in many plants,can reduce early brain injury after subarachnoid hemorrhage,but how it acts is still unclear.This study explored the mechanism using the experimental subarachnoid hemorrhage rat model established by injecting autologous blood into the cerebellomedullary cistern.Rat models were treated with an intraperitoneal injection of 60 mg/kg resveratrol 2,6,24 and 46 hours after injury.At 48 hours after injury,their neurological function was assessed using a modified Garcia score.Brain edema was measured by the wet-dry method.Neuronal apoptosis in the prefrontal cortex was detected by terminal deoxyribonucleotidyl transferase-mediated biotin-16-dUTP nick-end labeling assay.Levels of reactive oxygen species and malondialdehyde in the prefrontal cortex were determined by colorimetry.CHOP,glucose-regulated protein 78,nuclear factor-erythroid2-related factor 2 and heme oxygenase-1 mRNA expression levels in the prefrontal cortex were measured by reverse transcription polymerase chain reaction.Tumor necrosis factor-alpha content in the prefrontal cortex was detected by enzyme linked immunosorbent assay.Immunohistochemical staining was used to detect the number of positive cells of nuclear factor-erythroid 2-related factor 2,heme oxygenase 1,glucose-regulated protein 78,CHOP and glial fibrillary acidic protein.Western blot assay was utilized to analyze the expression levels of nuclear factor-erythroid 2-related factor 2,heme oxygenase 1,glucose-regulated protein 78 and CHOP protein expression levels in the prefrontal cortex.The results showed that resveratrol treatment markedly alleviated neurological deficits and brain edema in experimental subarachnoid hemorrhage rats,and reduced neuronal apoptosis in the prefrontal cortex.Resveratrol reduced the levels of reactive oxygen species and malondialdehyde,and increased the expression of nuclear factor-erythroid 2-related factor 2,heme oxygenase-1 mRNA and protein in the prefrontal cortex.Resveratrol 展开更多
关键词 nerve REGENERATION RESVERATROL oxidative STRESS endoplasmic reticulum STRESS neuroinflammation SUBARACHNOID hemorrhage nuclear factor-erythroid 2-related FACTOR 2 heme oxygenase-1 glucose-regulated protein 78 neural REGENERATION
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瑞芬太尼改善异氟醚致新生大鼠神经毒性的机制 预览
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作者 郭莹 潘波 黄绍强 《复旦学报:医学版》 CAS CSCD 北大核心 2019年第1期8-13,共6页
目的研究瑞芬太尼对异氟醚引起的新生大鼠海马神经毒性急性期和远期影响及其可能机制。方法将出生7天的大鼠随机分成4组:对照组(Sham组)、异氟醚组(Iso组)、异氟醚+切开组(Iso+I组)及异氟醚+切开+瑞芬太尼组(Ref组),采用每天2 h连续3天... 目的研究瑞芬太尼对异氟醚引起的新生大鼠海马神经毒性急性期和远期影响及其可能机制。方法将出生7天的大鼠随机分成4组:对照组(Sham组)、异氟醚组(Iso组)、异氟醚+切开组(Iso+I组)及异氟醚+切开+瑞芬太尼组(Ref组),采用每天2 h连续3天的处理方式模拟临床多次麻醉暴露。在第3天麻醉结束后 6 h取新鲜海马组织用Western blot检测NF-κB p65蛋白入核的比例,q-RT-PCR检测炎症因子IL-1β、IL-6和 TNF-α的mRNA的相对表达量;灌注取脑后用免疫荧光计数离子钙接头蛋白抗原分子-1 (ionized calcium binding adaptor molecule 1,IBA1)阳性细胞数量。大鼠在出生后的第65天进行被动回避实验,观察其学习与记忆能力。结果与Sham组相比,Iso组和Iso+Ⅰ组NF-κB p65蛋白入核的比例显著增加,IL-1β与TNF-α的mRNA的表达量上调,而且这种神经毒性在幼鼠成年后表现为学习与记忆障碍,然而瑞芬太尼显著改善由异氟醚多次暴露所致的神经炎症反应及学习记忆障碍。结论瑞芬太尼改善异氟醚致新生大鼠神经炎症反应,可能通过NF-κB p65通路发挥作用。 展开更多
关键词 发育大脑 瑞芬太尼 异氟醚 神经炎症
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尿酸激活Nrf2-ARE信号通路对帕金森病小鼠的保护作用 预览
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作者 黄婷婷 郝冬琳 +2 位作者 吴波娜 毛伦林 张金 《安徽医药》 CAS 2019年第7期1315-1319,I0002共6页
目的探讨尿酸对帕金森病(PD)小鼠的神经保护作用以及对核因子E2相关因子2(Nrf2)的调控作用。方法雄性C57BL/6J小鼠(6~8周、20~25 g)30只,采用随机数字表法分为三组:对照组(生理盐水)、1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)组、尿酸组(... 目的探讨尿酸对帕金森病(PD)小鼠的神经保护作用以及对核因子E2相关因子2(Nrf2)的调控作用。方法雄性C57BL/6J小鼠(6~8周、20~25 g)30只,采用随机数字表法分为三组:对照组(生理盐水)、1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)组、尿酸组(尿酸+MPTP),每组各10只。MPTP组小鼠经腹腔注射MPTP(20 mg/kg),每天1次,连续7 d。尿酸组于MPTP给药之前2 h腹腔注射尿酸(250 mg/kg),共13 d(MPTP注射前3 d,MPTP注射同时的7 d,MPTP结束后3 d)。对照组接受0.9%生理盐水代替MPTP和尿酸。在第14天测量各组小鼠的行为和认知功能,处死小鼠获取脑组织,免疫荧光染色测定黑质酪氨酸羟化酶(TH)的表达。实时荧光定量PCR检测Nrf2及下游基因mRNA的表达。免疫组化检测海马白细胞介素-1β(IL-1β)表达。酶联免疫吸附试验(ELISA)检测血清和海马IL-1β、白细胞介素-6(IL-6)和肿瘤坏死因子-α(TNF-α)水平。结果尿酸能改善PD小鼠的行为学和认知功能,增加黑质TH阳性多巴胺能神经元数目和纹状体多巴胺含量。尿酸增加Nrf2和Nrf2下游基因mRNA的表达,包括γ-GCLC、HO-1和NQO1。尿酸显著提高MPTP处理小鼠黑质区SOD、CAT、GSH含量,降低MDA含量。尿酸抑制海马组织IL-1β蛋白的表达,并降低血清和海马中IL-1β、IL-6和TNF-α水平。结论尿酸对PD小鼠多巴胺能神经元显示神经保护特性,其机制可能与尿酸通过激活Nrf2-ARE通路及调节神经炎症和氧化应激有关。 展开更多
关键词 帕金森病 尿酸 氧化应激 神经炎症 核因子E2相关因子2 黑质 多巴胺能神经元
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Choroid plexus tumor necrosis factor receptor 1:a new neuroinflammatory piece of the complex Alzheimer’s disease puzzle 预览
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作者 Sophie Steeland Roosmarijn E.Vandenbroucke 《中国神经再生研究:英文版》 SCIE CAS CSCD 2019年第7期1144-1147,共4页
Due to the aging of the population and despite the enormous scientific effort,Alzheimer’s disease remains one of the biggest medical and pharmaceutical challenges in current medicine.Novel insights highlight the impo... Due to the aging of the population and despite the enormous scientific effort,Alzheimer’s disease remains one of the biggest medical and pharmaceutical challenges in current medicine.Novel insights highlight the importance of neuroinflammation as an undeniable player in the onset and progression of Alzheimer’s disease.Tumor necrosis factor is a master inflammatory cytokine that signals via tumor necrosis factor receptor 1 and tumor necrosis factor receptor 2,but that also regulates several brain functions in health and disease.However,clinical trials investigating drugs that interfere with the tumor necrosis factor pathway in Alzheimer’s disease led to inconclusive results,partially because not only the pro-inflammatory tumor necrosis factor/tumor necrosis factor receptor 1,but also the beneficial tumor necrosis factor/tumor necrosis factor receptor 2 signaling was antagonized in these trials.We recently found that tumor necrosis factor is the main upregulated cytokine in the choroid plexus of Alzheimer’s disease patients,signaling via tumor necrosis factor receptor 1.In agreement with this,choroidal tumor necrosis factor/tumor necrosis factor receptor 1 signaling was also upregulated in different Alzheimer’s disease mouse models.Interestingly,both genetic and nanobody-based pharmacological blockage of tumor necrosis factor receptor 1 signaling was accompanied by favorable effects on Alzheimer’s disease-associated inflammation,choroidal morphology and cognitive functioning.Here,we briefly summarize the detrimental effects that can be mediated by tumor necrosis factor/tumor necrosis factor receptor 1 signaling in(early)Alzheimer’s disease,and the consequences this might have on the disease progression.As the main hypothesis in Alzheimer’s disease clinical trials is still based on the amyloid beta-cascade,the importance of Alzheimer’s disease-associated neuroinflammation urge the development of novel therapeutic strategies that might be effective in the early stages of Alzheimer’s disease and pr 展开更多
关键词 tumor necrosis factor NEUROINFLAMMATION blood-cerebrospinal fluid barrier PRECLINICAL research drug development NEURODEGENERATION cognitive decline mouse models TNFR
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氧化应激与帕金森病 预览
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作者 朱羽婷 朱向阳 +1 位作者 周永 张冬梅 《中国实用神经疾病杂志》 2019年第11期1271-1276,共6页
帕金森病(Parkinson’s disease,PD)是一种逐渐进展的与年龄相关的神经系统退行性疾病,随着社会人口老龄化,其发病率逐年增高。PD主要病理特征为中脑黑质致密部多巴胺能神经元的缺失及路易小体形成。其病因目前尚不完全清楚,目前认为是... 帕金森病(Parkinson’s disease,PD)是一种逐渐进展的与年龄相关的神经系统退行性疾病,随着社会人口老龄化,其发病率逐年增高。PD主要病理特征为中脑黑质致密部多巴胺能神经元的缺失及路易小体形成。其病因目前尚不完全清楚,目前认为是由于遗传易感性、环境毒素和衰老等几种因素共同相互作用的结果。研究证实,PD患者大脑黑质中多巴胺能神经元的变性或(和)死亡与氧化应激关系较为密切。本文就PD与氧化应激近年来的研究进展做一综述。 展开更多
关键词 帕金森病 氧化应激 保护机制 多巴胺神经元 神经炎症 线粒体功能障碍
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Potential therapeutic roles of retinoids for prevention of neuroinflammation and neurodegeneration in Alzheimer’s disease 预览
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作者 Bhaskar C. Das Somsankar Dasgupta Swapan K. Ray 《中国神经再生研究:英文版》 SCIE CAS CSCD 2019年第11期1880-1892,共13页
All retinoids, which can be natural and synthetic, are chemically related to vitamin A. Both natural and synthetic retinoids use specific nuclear receptors such as retinoic acid receptors and retinoid X receptors to a... All retinoids, which can be natural and synthetic, are chemically related to vitamin A. Both natural and synthetic retinoids use specific nuclear receptors such as retinoic acid receptors and retinoid X receptors to activate specific signaling pathways in the cells. Retinoic acid signaling is extremely important in the central nervous system. Impairment of retinoic acid signaling pathways causes severe pathological processes in the central nervous system, especially in the adult brain. Retinoids have major roles in neural patterning, differentiation, axon outgrowth in normal development, and function of the brain. Impaired retinoic acid signaling results in neuroinflammation, oxidative stress, mitochondrial malfunction, and neurodegeneration leading to progressive Alzheimer’s disease, which is pathologically characterized by extra-neuronal accumulation of amyloid plaques(aggregated amyloid-beta) and intra-neurofibrillary tangles(hyperphosphorylated tau protein) in the temporal lobe of the brain. Alzheimer’s disease is the most common cause of dementia and loss of memory in old adults. Inactive cholinergic neurotransmission is responsible for cognitive deficits in Alzheimer’s disease patients. Deficiency or deprivation of retinoic acid in mice is associated with loss of spatial learning and memory. Retinoids inhibit expression of chemokines and neuroinflammatory cytokines in microglia and astrocytes, which are activated in Alzheimer’s disease. Stimulation of retinoic acid receptors and retinoid X receptors slows down accumulation of amyloids, reduces neurodegeneration, and thereby prevents pathogenesis of Alzheimer’s disease in mice. In this review, we described chemistry and biochemistry of some natural and synthetic retinoids and potentials of retinoids for prevention of neuroinflammation and neurodegeneration in Alzheimer’s disease. 展开更多
关键词 Alzheimer's disease amyloid PLAQUES neurofibrillary TANGLES NEUROINFLAMMATION NEURODEGENERATION RETINOIDS
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电针“委中”对多裂肌损伤大鼠MG激活的影响 预览
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作者 白玉琢 徐菁 +6 位作者 陈洁 张佳怡 许玥 鲁曼 李欣怡 霍则军 张莉 《针灸临床杂志》 2019年第5期62-66,共5页
目的:探讨电针“委中”对多裂肌损伤后小胶质细胞激活介导的神经炎症的治疗机制。方法:SD大鼠随机分为空白组、模型1天组、模型3天组、电针1天组、电针3天组,每组各8只。电针组双侧“委中”电针,治疗的1天、3天后同步取材。结果:模型1... 目的:探讨电针“委中”对多裂肌损伤后小胶质细胞激活介导的神经炎症的治疗机制。方法:SD大鼠随机分为空白组、模型1天组、模型3天组、电针1天组、电针3天组,每组各8只。电针组双侧“委中”电针,治疗的1天、3天后同步取材。结果:模型1天组和3天组多裂肌IL-6、TNF-α、iNOS、脊髓和海马iNOS含量较空白组显著升高(P<0.01);电针1天组多裂肌IL-6、TNF-α、iNOS含量降低(P<0.01),脊髓和海马iNOS含量较模型1天组显著降低(P<0.01);电针3天组多裂肌IL-6、iNOS含量降低(P>0.05),脊髓和海马iNOS含量较模型3天组未见统计学差异,多裂肌TNF-α含量显著低于模型3天组(P<0.01)。结论:电针“委中”对腰多裂肌损伤模型大鼠损伤初期的神经炎症干预效果较佳,可能与其降低外周和中枢炎性因子IL-6、TNF-α、iNOS含量,抑制M1型小胶质细胞的过度激活有关。 展开更多
关键词 多裂肌 小胶质细胞 神经炎症 脊髓 海马
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L-Norvaline,a new therapeutic agent against Alzheimer’s disease 预览
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作者 Baruh Polis Kolluru D.Srikanth +2 位作者 Vyacheslav Gurevich Hava Gil-Henn Abraham O.Samson 《中国神经再生研究:英文版》 SCIE CAS CSCD 2019年第9期1562-1572,共11页
Growing evidence highlights the role of arginase activity in the manifestation of Alzheimer’s disease(AD).Upregulation of arginase was shown to contribute to neurodegeneration.Regulation of arginase activity appears ... Growing evidence highlights the role of arginase activity in the manifestation of Alzheimer’s disease(AD).Upregulation of arginase was shown to contribute to neurodegeneration.Regulation of arginase activity appears to be a promising approach for interfering with the pathogenesis of AD.Therefore,the enzyme represents a novel therapeutic target.In this study,we administered an arginase inhibitor,L-norvaline(250 mg/L),for 2.5 months to a triple-transgenic model(3×Tg-AD)harboring PS1M146V,APPSwe,and tauP301L transgenes.Then,the neuroprotective effects of L-norvaline were evaluated using immunohistochemistry,proteomics,and quantitative polymerase chain reaction assays.Finally,we identified the biological pathways activated by the treatment.Remarkably,L-norvaline treatment reverses the cognitive decline in AD mice.The treatment is neuroprotective as indicated by reduced beta-amyloidosis,alleviated microgliosis,and reduced tumor necrosis factor transcription levels.Moreover,elevated levels of neuroplasticity related postsynaptic density protein 95 were detected in the hippocampi of mice treated with L-norvaline.Furthermore,we disclosed several biological pathways,which were involved in cell survival and neuroplasticity and were activated by the treatment.Through these modes of action,L-norvaline has the potential to improve the symptoms of AD and even interferes with its pathogenesis.As such,L-norvaline is a promising neuroprotective molecule that might be tailored for the treatment of a range of neurodegenerative disorders.The study was approved by the Bar-Ilan University Animal Care and Use Committee(approval No.82-10-2017)on October 1,2017. 展开更多
关键词 DEMENTIA ARGINASE inhibition ARGININE urea cycle microgliosis NEUROINFLAMMATION cytokines tumor necrosis factor mTOR NEURODEGENERATION
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小续命汤提取物下调TLR4/MyD88信号通路减轻脂多糖诱导神经炎症的体内外研究(英文)
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作者 程笑 杨欢 +4 位作者 杨滢霖 李伟瀚 刘漫 王月华 杜冠华 《中国药学:英文版》 CAS CSCD 2019年第2期88-99,共12页
探讨小续命汤提取物(Xiao-Xu-Ming decoction extract, XXM)对脂多糖(lipopolysaccaride, LPS)诱导的体内外神经炎症的影响。体外实验应用200 ng/mLLPS处理BV2小胶质细胞24小时以诱导炎症反应。体内实验应用5 mg/kgLPS诱导小鼠炎症反应... 探讨小续命汤提取物(Xiao-Xu-Ming decoction extract, XXM)对脂多糖(lipopolysaccaride, LPS)诱导的体内外神经炎症的影响。体外实验应用200 ng/mLLPS处理BV2小胶质细胞24小时以诱导炎症反应。体内实验应用5 mg/kgLPS诱导小鼠炎症反应。Griess试剂测定NO含量;ELISA法测定IL-1β、IL-6、TNF-α和MCP-1的含量;WB检测Iba-1、TLR4和MyD88蛋白的表达;RT-PCR测定TLR4和MyD88的mR NA水平。结果发现,在体外细胞上, XXM显著降低LPS诱导的BV2细胞上清液中NO、IL-1β、IL-6和TNF-α的水平增高,抑制LPS诱导的BV2细胞中炎症蛋白TLR4和MyD88的表达。在小鼠脑皮层组织中,XXM显著抑制LPS诱导的小胶质细胞活化,降低LPS诱导的炎症因子和趋化因子IL-1β、IL-6、TNF-α和MCP-1的水平增高,抑制LPS诱导的TLR4和MyD88蛋白的表达。结果表明,XXM可下调TLR4/MYD88信号通路来减轻LPS诱导的神经炎症反应。 展开更多
关键词 小续命汤 脂多糖 BV2细胞 神经炎症 TOLL样受体4
Differences in pathological changes between two rat models of severe traumatic brain injury 预览
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作者 Yi-Ming Song Yu Qian +6 位作者 Wan-Qiang Su Xuan-Hui Liu Jin-Hao Huang Zhi-Tao Gong Hong-Liang Luo Chuang Gao Rong-Cai Jiang 《中国神经再生研究:英文版》 SCIE CAS CSCD 2019年第10期1796-1804,共9页
The rat high-impact free weight drop model mimics the diffuse axonal injury caused by severe traumatic brain injury in humans,while severe controlled cortical impact can produce a severe traumatic brain injury model u... The rat high-impact free weight drop model mimics the diffuse axonal injury caused by severe traumatic brain injury in humans,while severe controlled cortical impact can produce a severe traumatic brain injury model using precise strike parameters.In this study,we compare the pathological mechanisms and pathological changes between two rat severe brain injury models to identify the similarities and differences.The severe controlled cortical impact model was produced by an electronic controlled cortical impact device,while the severe free weight drop model was produced by dropping a 500 g free weight from a height of 1.8 m through a plastic tube.Body temperature and mortality were recorded,and neurological deficits were assessed with the modified neurological severity score.Brain edema and bloodbrain barrier damage were evaluated by assessing brain water content and Evans blue extravasation.In addition,a cytokine array kit was used to detect inflammatory cytokines.Neuronal apoptosis in the brain and brainstem was quantified by immunofluorescence staining.Both the severe controlled cortical impact and severe free weight drop models exhibited significant neurological impairments and body temperature fluctuations.More severe motor dysfunction was observed in the severe controlled cortical impact model,while more severe cognitive dysfunction was observed in the severe free weight drop model.Brain edema,inflammatory cytokine changes and cortical neuronal apoptosis were more substantial and blood-brain barrier damage was more focal in the severe controlled cortical impact group compared with the severe free weight drop group.The severe free weight drop model presented with more significant apoptosis in the brainstem and diffused blood-brain barrier damage,with higher mortality and lower repeatability compared with the severe controlled cortical impact group.Severe brainstem damage was not found in the severe controlled cortical impact model.These results indicate that the severe controlled cortical impact model is relat 展开更多
关键词 nerve REGENERATION severe traumatic brain INJURY animal model comparison free weight drop controlled cortical impact NEUROLOGICAL impairment NEUROINFLAMMATION blood-brain barrier damage neuronal apoptosis diffuse AXONAL INJURY BRAINSTEM INJURY neural REGENERATION
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抗阿尔茨海默病药物研发进展
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作者 郑易林 谢琼 +3 位作者 肖立 李秋 徐丽丽 邵黎明 《药学进展》 CAS 2019年第2期100-110,共11页
阿尔茨海默病(AD)是一种常见的神经退行性疾病,患病人数众多,给家庭、社会带来沉重的经济负担。由于AD的发病机制尚未阐明,抗AD新药开发面临巨大挑战,迄今尚未找到治愈AD的有效治疗手段和药物。全球各大制药公司和研究机构均高度关注抗A... 阿尔茨海默病(AD)是一种常见的神经退行性疾病,患病人数众多,给家庭、社会带来沉重的经济负担。由于AD的发病机制尚未阐明,抗AD新药开发面临巨大挑战,迄今尚未找到治愈AD的有效治疗手段和药物。全球各大制药公司和研究机构均高度关注抗AD药物的研发进展,尤其是处于临床研究阶段的抗AD药物。根据药物作用靶点和机制,包括减少β-淀粉样蛋白、平衡Tau蛋白、调节神经递质、平衡Ca^2+水平、抗氧化应激、抑制炎性反应、调节糖代谢和激素水平等,对目前抗AD小分子药物临床研究的新进展进行综述。 展开更多
关键词 阿尔茨海默病 Β-淀粉样蛋白 TAU蛋白 神经递质 神经炎性反应 小分子药物
Ginsenoside Rb1 protects dopaminergic neurons from inflammatory injury induced by intranigral lipopolysaccharide injection 预览
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作者 Da-Wei Li Fa-Zhan Zhou +4 位作者 Xian-Chang Sun Shu-Chen Li Jin-Bin Yang Huan-Huan Sun Ai-Hua Wang 《中国神经再生研究:英文版》 SCIE CAS CSCD 2019年第10期1814-1822,共9页
Accumulating studies suggest that neuroinflammation characterized by microglial overactivation plays a pivotal role in the pathogenesis of Parkinson’s disease.As such,inhibition of microglial overactivation might be ... Accumulating studies suggest that neuroinflammation characterized by microglial overactivation plays a pivotal role in the pathogenesis of Parkinson’s disease.As such,inhibition of microglial overactivation might be a promising treatment strategy to delay the onset or slow the progression of Parkinson’s disease.Ginsenoside Rbl,the most active ingredient of ginseng,reportedly exerts neuroprotective effects by suppressing inflammation in vitro.The present study aimed to evaluate the neuroprotective and anti-inflammatory effects of ginsenoside Rbl in a lipopolysaccharide-induced rat Parkinson’s disease model.Rats were divided into four groups.In the control group,sham-operated rats were intraperitoneally administered normal saline for 14 consecutive days.In the ginsenoside Rbl group,ginsenoside Rb1(20 mg/kg)was intraperitoneally injected for 14 consecutive days after sham surgery.In the lipopolysaccharide group,a single dose of lipopolysaccharide was unilaterally microinjected into the rat substantial nigra to establish the Parkinson’s disease model.Lipopolysaccharide-injected rats were treated with normal saline for 14 consecutive days.In the ginsenoside Rbl +lipopolysaccharide group,lipopolysaccharide was unilaterally microinjected into the rat substantial nigra.Subsequently,ginsenoside Rbl was intraperitoneally injected for 14 consecutive days.To investigate the therapeutic effects of ginsenoside Rbl,behavioral tests were performed on day 15 after lipopolysaccharide injection.We found that ginsenoside Rbl treatment remarkably reduced apomorphine-induced rotations in lipopolysaccharide-treated rats compared with the lipopolysaccharide group.To investigate the neurotoxicity of lipopolysaccharide and potential protective effect of ginsenoside Rbl,contents of dopamine and its metabolites in the striatum were measured by high-performance liquid chromatography.Compared with the lipopolysaccharide group,ginsenoside Rbl obviously attenuated the lipopolysaccharide-induced depletion of dopamine and its metabolites 展开更多
关键词 nerve REGENERATION NEURODEGENERATION Parkinson's disease GINSENOSIDE Rb1 neuroinflammation LIPOPOLYSACCHARIDE DOPAMINERGIC neuron microglia nuclear factor kappa B dopamine tyrosine HYDROXYLASE substantia nigra neural REGENERATION
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瓜子金皂苷己抑制IL-1β的释放及其机制研究 预览
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作者 龙倩 王莎莎 +3 位作者 邵千航 苑玉和 贺文彬 陈乃宏 《中国药理学通报》 CAS CSCD 北大核心 2019年第5期668-673,共6页
目的研究瓜子金皂苷己(polygalasaponin F,PS-F)对LPS诱导的BV2小胶质细胞炎症反应中炎性因子IL-1β释放的影响及其作用机制。方法实验分为空白组、LPS模型组、LPS+PS-F (0.10、1.00、10.00 μmol·L-1 )给药组。运用ELISA法检测培... 目的研究瓜子金皂苷己(polygalasaponin F,PS-F)对LPS诱导的BV2小胶质细胞炎症反应中炎性因子IL-1β释放的影响及其作用机制。方法实验分为空白组、LPS模型组、LPS+PS-F (0.10、1.00、10.00 μmol·L-1 )给药组。运用ELISA法检测培养液上清中IL-1β的分泌量;real-time PCR检测IL-1β mRNA的表达;Western blot检测 IL-1β、NLRP3、caspase-1、ASC、caspase-11的蛋白表达量。结果 ELISA、real-time PCR和Western blot结果均表明,PS-F能有效抑制LPS诱导BV2小胶质细胞释放炎性因子IL-1β( P <0.01, P <0.05);Western blot结果表明,PS-F可以下调NLRP3、caspase-1、ASC、caspase-11的蛋白表达,其中ASC、caspase-11所得结果差异有统计学意义( P <0.05)。结论 PS-F可以有效抑制LPS诱导BV2细胞炎症反应中炎性因子IL-1β的释放,且与下调 NLRP3炎性小体、抑制caspase-11的激活有关。 展开更多
关键词 瓜子金皂苷己 脂多糖 神经炎症 IL-1Β 炎性小体 BV2细胞
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Menin:一个新的神经系统疾病防治靶点
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作者 朱慰文 杨三桥 唐小卿 《中南药学》 CAS 2019年第6期889-894,共6页
Menin蛋白是MEN1基因编码的产物,可通过调控突触可塑性和神经炎症发挥神经保护作用。神经炎症的发生和突触可塑性障碍被证明参与大多数神经系统疾病的发病过程,因此开发抑制神经炎症和改善突触可塑性的药物对治疗神经系统疾病具有重要... Menin蛋白是MEN1基因编码的产物,可通过调控突触可塑性和神经炎症发挥神经保护作用。神经炎症的发生和突触可塑性障碍被证明参与大多数神经系统疾病的发病过程,因此开发抑制神经炎症和改善突触可塑性的药物对治疗神经系统疾病具有重要意义。所以本文将综述Menin在神经系统疾病相关症状中的调节作用及潜在机制,并展望Menin对阿尔兹海默症和帕金森病等神经退行性疾病的潜在防治作用。 展开更多
关键词 MENIN蛋白 神经系统疾病 神经炎症 突触可塑性
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