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Therapeutic effect and psychological impact of aspirin plus edaravone on patients with cerebral infarction
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作者 Tian-Shu Wang Li-Jun Jing 《World Journal of Psychiatry》 SCIE 2024年第5期644-652,共9页
BACKGROUND Cerebral infarction(CI)is characterized by a high prevalence,disability,and mortality.Timely or improper treatment greatly affects patient prognosis.AIM To explore the drug efficacy of aspirin plus edaravon... BACKGROUND Cerebral infarction(CI)is characterized by a high prevalence,disability,and mortality.Timely or improper treatment greatly affects patient prognosis.AIM To explore the drug efficacy of aspirin plus edaravone and to explore their effect on quality of life(QOL),anxiety and depression in CI patients.METHODS We retrospectively analyzed the records of 124 CI patients treated between June 2019 and February 2021 who were assigned to an observation group(OG)(combination therapy of aspirin and edaravone,65 patients)or a control group(CG)(aspirin monotherapy,59 patients).The therapeutic effects,pre-and posttreatment National Institutes of Health Stroke Scale(NIHSS)scores,activities of daily living,degree of cognitive impairment,protein levels of glial fibrillary acidic protein(GFAP),neuron-specific enolase(NSE)and S-100B,occurrence of adverse reactions,and serum high-sensitivity C-reactive protein(hs-CRP),interleukin(IL)-6 and tumor necrosis factor(TNF)-αwere evaluated,detected and compared between the two groups.Finally,posttreatment QOL,anxiety,and depression were assessed by the Medical Outcomes Study 36-Item Short Form Health Survey Scale,Self-rating Depression Scale(SDS),and Self-rating Anxiety Scale(SAS),respectively.RESULTS Compared with the CG,the OG had markedly better therapeutic effects,greater improvements in activities of daily living,and better alleviation in cognitive dysfunction after treatment,as well as lower posttreatment NIHSS scores and serum NSE,GFAP,S-100B,hs-CRP,IL-6,and TNF-αlevels;the OG was similar to the CG in terms of adverse reactions but was better than the CG in terms of posttreatment QOL;and the OG also had lower SDS and SAS scores than the CG after treatment.CONCLUSION Aspirin plus edaravone had a good curative effect on CI.It can reverse cranial nerve damage in patients,improve neurological function and prognosis,and alleviate inflammation,anxiety,and depression;thus,it is considered safe and worthy of clinical application. 展开更多
关键词 ASPIRIN edaravone Cerebral infarction EFFICACY Quality of life
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Edaravone administration and its potential association with a new clinical syndrome in cerebral infarction patients:Three case reports
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作者 Liu Yang Xin Xu +2 位作者 Liang Wang Ke-Bin Zeng Xue-Feng Wang 《World Journal of Clinical Cases》 SCIE 2023年第19期4648-4654,共7页
BACKGROUND Edaravone is a widely used treatment for patients with cerebral infarction and,in most cases,edaravone-induced side effects are mild.However,edaravone-related adverse reactions have been receiving increasin... BACKGROUND Edaravone is a widely used treatment for patients with cerebral infarction and,in most cases,edaravone-induced side effects are mild.However,edaravone-related adverse reactions have been receiving increasing attention.CASE SUMMARY We treated three patients with acute cerebral infarction who died following treatment with edaravone.Edaravone is a widely used treatment for patients with cerebral infarction and,in most cases,edaravone-induced side effects are mild.However,edaravone-related adverse reactions have been receiving increasing attention.CONCLUSION Our cases highlight the importance of educating clinicians regarding the new edaravone-induced clinical syndromes of cerebral infarction as potentially fatal adverse drug reactions.Considering that no laboratory or confirmatory test exists to diagnose edaravone-induced death from cerebral infarction,clinicians’knowledge is the key element in recognizing this phenomenon. 展开更多
关键词 edaravone Sudden death PATIENTS Cerebral infarction Case report
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Edaravone对视网膜缺血-再灌注损伤大鼠Bcl-2和Bax表达的影响 被引量:3
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作者 梁冰 曹永亮 +3 位作者 郭爱华 李娜娜 韩延燕 曲群 《眼科新进展》 CAS 北大核心 2013年第4期316-318,共3页
目的研究Edaravone对视网膜缺血-再灌注损伤(retinal ischem ia-reperfusion injury,RIRI)大鼠视网膜神经节细胞Bc-l2和Bax表达的影响。方法健康Wistar大鼠36只随机分为3组:空白对照组、模型组和Edaravone治疗组。空白对照组不做任何处... 目的研究Edaravone对视网膜缺血-再灌注损伤(retinal ischem ia-reperfusion injury,RIRI)大鼠视网膜神经节细胞Bc-l2和Bax表达的影响。方法健康Wistar大鼠36只随机分为3组:空白对照组、模型组和Edaravone治疗组。空白对照组不做任何处理,模型组和Edaravone治疗组均采用前房加压法建立大鼠RIRI模型,Edaravone治疗组于缺血前30min行腹腔注射Edaravone(3mg.kg-1),恢复灌注30min后再行腹腔注射Edaravone(3mg.kg-1)。免疫组织化学法检测各组大鼠视网膜缺血-再灌注后24h视网膜神经节细胞Bc-l2和Bax的表达情况。结果空白对照组未见Bc-l2和Bax表达。再灌注后24h,模型组Bc-l2表达为0.406±0.022,Bax表达为0.661±0.034,Bc-l2/Bax为0.609±0.015;Edaravone治疗组Bc-l2表达为0.581±0.031,Bax表达为0.491±0.017,Bc-l2/Bax为1.104±0.094。与模型组比较,Edaravone治疗组Bc-l2表达明显增强(P<0.05),Bax表达明显减弱(P<0.05),Bc-l2/Bax比值升高(P<0.05)。结论 Edaravone对RIRI大鼠视网膜神经节细胞有明显的保护作用。 展开更多
关键词 edaravone 视网膜缺血-再灌注损伤 Bc-l2 BAX
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Edaravone对DBI大鼠脑组织超微结构及神经功能的影响 被引量:2
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作者 赵雅宁 张文丽 +2 位作者 田艳霞 崔建忠 高俊玲 《山东医药》 CAS 北大核心 2009年第2期15-17,共3页
目的研究弥漫性脑创伤(DBI)后依达拉奉(Edaravone)对大鼠脑组织超微结构及神经功能的影响。方法将雄性SD大鼠随机分为假手术组、创伤组、Edaravone治疗组。Marmarou′s法建立大鼠DBI损伤模型。术后24、48、72 h取大脑海马组织做电镜观察... 目的研究弥漫性脑创伤(DBI)后依达拉奉(Edaravone)对大鼠脑组织超微结构及神经功能的影响。方法将雄性SD大鼠随机分为假手术组、创伤组、Edaravone治疗组。Marmarou′s法建立大鼠DBI损伤模型。术后24、48、72 h取大脑海马组织做电镜观察;术后24、48、72 h对大鼠学习记忆功能(水迷宫法)和综合运动功能(转棒法)进行评定。结果电镜下Edaravone治疗组中神经元细胞核、线粒体受损程度均低于创伤组;水迷宫实验显示创伤组大鼠搜索安全岛潜伏期(230.9±20.9)s,假手术组为(50.7±4.9)s,Edaravone治疗组为(70.6±8.7)s,三组比较,P均<0.05;创伤组综合运动能力评分为(79.1±24.5)s,假手术组为(278.6±32.7)s,Edaravone治疗组为(130.0±30.8)s,三组比较,P均<0.05。结论Edaravone可改善DBI后学习记忆功能和综合运动功能,减轻海马神经元超微结构损害程度。 展开更多
关键词 弥漫性脑创伤 依达拉奉 超微结构 神经功能
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Edaravone对大鼠弥漫性脑创伤后ERK1/2通路的影响
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作者 赵雅宁 赵毓芳 +3 位作者 陈海红 崔建忠 饶颖臻 高俊玲 《神经解剖学杂志》 CAS CSCD 北大核心 2009年第1期91-95,共5页
为探讨Edaravone对脑创伤的保护机制,本研究观察了Edaravone对弥漫性脑创伤大鼠脑组织磷酸化细胞外信号调节激酶ERK1/2表达变化的影响。114只雄性SD大鼠,随机分为3组:(1)假手术对照组(A组,n=18),(2)创伤组(B组,n=48),(3)Edaravone治疗... 为探讨Edaravone对脑创伤的保护机制,本研究观察了Edaravone对弥漫性脑创伤大鼠脑组织磷酸化细胞外信号调节激酶ERK1/2表达变化的影响。114只雄性SD大鼠,随机分为3组:(1)假手术对照组(A组,n=18),(2)创伤组(B组,n=48),(3)Edaravone治疗组(C组,n=48),采用Marmarou’s法建立大鼠弥漫性颅脑损伤模型。伤后1、3、6、24、48和72h,HE染色观察伤后皮质和海马区神经细胞组织形态变化,Western blot法、免疫组化法检测皮质和海马区p-ERK1/2的表达,术后24、48、72h对大鼠神经运动功能和综合运动能力评分。结果显示:光镜下,伤后6、24h即可见B组大脑皮质和海马区神经细胞胞体收缩呈三角形,胞浆嗜色性减弱,核皱缩浓染,细胞周围出现空隙,即神经细胞变性坏死改变,C组上述改变明显减轻;免疫组化与Western blot法结果显示,与A组比较,B组ERK1/2(即p-ERK1/2)活性在伤后1、3、6、24、48h显著增高(P<0.05);与B组比较,C组中p-ERK1/2在6、24及48h显著回降(P<0.05);神经功能与综合运动能力评分在B组中(8.73±1.4,63.8±27.7)明显低于A组(24.00±0.00,278.4±27.7),C组(17.36±1.63,117.6±20.9)显著回升(P<0.05)。本研究表明Edaravone可改善脑创伤后神经功能损伤,其机制与调节脑创伤后ERK1/2信号活化水平有关。 展开更多
关键词 脑创伤 edaravone ERK1/2
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Edaravone对大鼠弥漫性脑创伤神经运动功能及脑组织超微结构的影响 被引量:1
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作者 赵雅宁 张文丽 +1 位作者 田艳霞 高俊玲 《第四军医大学学报》 北大核心 2009年第7期610-612,共3页
目的:研究依达拉奉(3-甲基-1-苯基-2-吡唑啉-5-酮,Edaravone)对大鼠弥漫性脑创伤神经功能损伤的治疗作用及其机制.方法:将148只雄性SD大鼠随机分为对照组、创伤组、Edaravone治疗组.采用Marmarous法建立大鼠弥漫性颅脑损伤模型,于术后6,... 目的:研究依达拉奉(3-甲基-1-苯基-2-吡唑啉-5-酮,Edaravone)对大鼠弥漫性脑创伤神经功能损伤的治疗作用及其机制.方法:将148只雄性SD大鼠随机分为对照组、创伤组、Edaravone治疗组.采用Marmarous法建立大鼠弥漫性颅脑损伤模型,于术后6,24h取大脑皮层冠状逢左右0.2cm组织脑组织作电镜观察,术后24,48,72h对大鼠神经运动功能和综合运动能力评分.结果:Edaravone治疗组大鼠死亡率(23%)明显低于创伤组(51%,P<0.05);电镜下,伤后6,24hEdara-vone治疗组中神经元内细胞器、轴索及毛细血管等超微结构的损伤程度明显低于创伤组;神经功能与综合运动能力评分在创伤组中(8.7±1.4,63.8±27.7)明显低于对照组(24.0±0.0,278.0±28.0);Edaravone治疗组(17.4±1.6,118.0±21.0)显著回升(P<0.05).结论:Edaravone可改善脑创伤后神经功能损伤,其机制与减轻脑创伤后脑组织超微结构损害有关. 展开更多
关键词 弥漫性脑创伤 3-甲基-1-苯基-2-吡唑啉-5-酮 超微结构
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Edaravone对大鼠脑创伤后ERK1/2信号通路及神经细胞凋亡的影响 被引量:1
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作者 赵雅宁 邓银侠 +2 位作者 崔建忠 张宇新 高俊玲 《基础医学与临床》 CSCD 北大核心 2009年第9期933-937,共5页
目的探讨Edaravone对脑创伤后ERK1/2信号通路及神经细胞凋亡的影响及其机制。方法用Marmarou s法建立SD大鼠中度弥漫性轴索损伤模型(n=120),随机分为3组:(1)假手术对照组(A组,n=24)、(2)创伤组(B组,n=48)、(3)Edaravone干... 目的探讨Edaravone对脑创伤后ERK1/2信号通路及神经细胞凋亡的影响及其机制。方法用Marmarou s法建立SD大鼠中度弥漫性轴索损伤模型(n=120),随机分为3组:(1)假手术对照组(A组,n=24)、(2)创伤组(B组,n=48)、(3)Edaravone干预组(C组,n=48)。分别在伤后1、6、24、48和72 h 5个时相点收取脑组织标本,硫代巴比妥酸法检测大脑皮质中MDA含量;Western-blot法检测皮质区p-ERK1/2活性;免疫组化法检测p-ERK1/2、BAX和BCL-2蛋白的表达;TUNEL法标记神经细胞凋亡数。计算机图像分析系统进行定量分析。结果与假手术组比较,创伤组中MDA含量(伤后6~72 h)、ERK1/2(p-ERK1/2)活性(伤后1~48 h)、BAX/BCL-2比值(伤后6~48 h)及凋亡的神经细胞数目(伤后6~72 h)显著增高(P〈0.05);Edaravone干预显著缓解上述改变(P〈0.05)。结论Edaravone可减少脑创伤后的神经细胞凋亡,其机制与其可清除氧自由基、抑制ERK1/2通路活化有关。 展开更多
关键词 脑创伤 依达拉奉 细胞外信号调节激酶1/2 细胞凋亡
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Edaravone对脊髓神经细胞体外存活的作用
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作者 郭伟韬 曾荣 +1 位作者 孙欣 刘双意 《中国医药导报》 CAS 2006年第21期1-2,共2页
目的探讨Edaravone对脊髓神经细胞体外存活的作用和对谷氨酸兴奋性神经细胞毒性的影响。方法分离培养脊髓背根神经节(DRG),加入谷氨酸并使用Edaravone进行干预,倒置显微镜下观测细胞在不同培养条件下存活;流式细胞仪观测分析神经细胞凋... 目的探讨Edaravone对脊髓神经细胞体外存活的作用和对谷氨酸兴奋性神经细胞毒性的影响。方法分离培养脊髓背根神经节(DRG),加入谷氨酸并使用Edaravone进行干预,倒置显微镜下观测细胞在不同培养条件下存活;流式细胞仪观测分析神经细胞凋亡。结果谷氨酸可诱导体外培养的DRG细胞凋亡,Edaravone抑制谷氨酸的神经细胞损伤作用,且浓度更高作用明显。结论Edaravone对谷氨酸的兴奋性神经细胞毒性具有浓度依赖性保护作用,其作用机制可能与其抗自由基导致的细胞凋亡有关。 展开更多
关键词 edaravone 谷氨酸 神经保护作用 脊髓背根神经节
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结膜下注射自由基清除剂Edaravone治疗大鼠视网膜静脉阻塞
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作者 姜彩辉 张卯年 瓶井资弘 《眼科新进展》 CAS 北大核心 2009年第11期829-831,共3页
目的探讨自由基清除剂Edaravone对大鼠视网膜静脉阻塞后脂质过氧化反应和炎症因子的抑制作用。方法利用孟加拉玫瑰红联合氩激光制备大鼠视网膜静脉阻塞模型并经眼底血管荧光造影确认。将眼底血管荧光造影显示完全阻塞的眼随机分为2组,每... 目的探讨自由基清除剂Edaravone对大鼠视网膜静脉阻塞后脂质过氧化反应和炎症因子的抑制作用。方法利用孟加拉玫瑰红联合氩激光制备大鼠视网膜静脉阻塞模型并经眼底血管荧光造影确认。将眼底血管荧光造影显示完全阻塞的眼随机分为2组,每组18眼。在激光照射后1 h,治疗组结膜下注射Edaravone 300μg(0.2 mL),对照组结膜下注射0.2 mL BSS。每天1次,共3~7 d。术后第3天、第7天摘除眼球制备行病理检查和视网膜匀浆,定量测定视网膜组织中丙二醛及白细胞介素-6(interleukin-6,IL-6)的含量。结果静脉阻塞成功后,阻塞部位远端的视网膜静脉立刻出现淤曲、扩张、动脉变细。阻塞后短时间内即出现渗出性视网膜脱离,并逐渐出现视网膜出血、水肿和玻璃体出血。视网膜静脉阻塞第3天,治疗组和对照组视网膜组织中丙二醛的含量分别为272.50 nmol.g-1和352.65 nmol.g-1(视网膜湿质量,P=0.003 5);第7天分别为217.50nmol.g-1和318.33 nmol.g-1(视网膜湿质量,P=0.017 7)。视网膜静脉阻塞第3天,治疗组和对照组视网膜组织中IL-6的含量分别为15.67 ng.g-1和22.67 ng.g-1(视网膜湿质量,P=0.003 7);第7天分别为17.17 ng.g-1和25.50 ng.g-1(视网膜湿质量,P=0.004 8)。结论Edaravone能够抑制视网膜静脉阻塞造成的急性缺血所致的脂质过氧化反应,同时又能抑制炎症因子的产生。因此,Edaravone有望成为新的治疗视网膜静脉阻塞的药物。 展开更多
关键词 edaravone 视网膜静脉阻塞 活性氧 促炎细胞因子
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脑创伤后Edaravone脑保护作用机制的实验研究
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作者 尹立国 崔建忠 +1 位作者 高俊玲 赵雅宁 《河北医药》 CAS 2015年第3期353-355,共3页
目的探讨Edaravone对脑创伤后保护作用的可能机制。方法采用改进的Marmarou’s法建立大鼠中度闭合性弥漫性颅脑损伤模型,应用TAB法、免疫组化,TUNEL法对大鼠伤后皮质自由基、细胞色素C及凋亡细胞数进行动态观察。结果伤后给予Edaravone... 目的探讨Edaravone对脑创伤后保护作用的可能机制。方法采用改进的Marmarou’s法建立大鼠中度闭合性弥漫性颅脑损伤模型,应用TAB法、免疫组化,TUNEL法对大鼠伤后皮质自由基、细胞色素C及凋亡细胞数进行动态观察。结果伤后给予Edaravone能明显减少自由基水平,降低细胞色素c表达和神经元细胞凋亡数。结论 Edaravone对颅脑创伤有治疗作用,其机制之一是通过减少自由基生成,抑制线粒体膜通透性转换孔(MPTP)开放,减少细胞色素c释放,进而减少神经细凋亡。 展开更多
关键词 脑创伤 edaravone 自由基 线粒体膜通透性转换孔 细胞色素C 凋亡
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Neuroprotective effect of edaravone in experimental glaucoma model in rats: a immunofluorescence and biochemical analysis 被引量:2
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作者 Arzu Toruk Aksar Nursen Yuksel +2 位作者 Mustafa Gok Mustafa Cekmen Yusuf Caglar 《International Journal of Ophthalmology(English edition)》 SCIE CAS 2015年第2期239-244,共6页
AIM: To evaluate the neuroprotective activity of systemically administered edaravone in early and late stage of experimental glaucoma in rats.METHODS: In this study, 60 Wistar albino rats were used. Experimental glauc... AIM: To evaluate the neuroprotective activity of systemically administered edaravone in early and late stage of experimental glaucoma in rats.METHODS: In this study, 60 Wistar albino rats were used. Experimental glaucoma model was created by injecting hyaluronic acid to the anterior chamber once a week for 6wk in 46 of 60 subjects. Fourteen subjects without any medication were included as control group.Edaravone administered intraperitoneally 3 mg/kg/d to the 15 of 30 subjects starting at the onset of glaucoma induction and also administered intraperitoneally3 mg/kg/d to the other 15 subjects starting at three weeks after the onset of glaucoma induction. The other16 subjects who underwent glaucoma induction was administered any therapy. Retinal ganglion cells(RGCs)have been marked with dextran tetramethylrhodamine(DTMR) retrograde at the end of the sixth week and after48 h, subjects were sacrificed by the method of cardiac perfusion. Alive RGC density was assessed in the wholemount retina. Whole-mount retinal tissues homogenized and nitric oxide(NO), malondialdehyde(MDA) and total antioxidant capacity(TAC) values were measured biochemically.RESULTS: RGCs counted with Image-Pro Plus program, in the treatment group were found to be statistically significantly protected, compared to the glaucoma group(Bonferroni,P 【0.05). The neuroprotective activity of edaravone was found to be more influential byadministration at the start of the glaucoma process.Statistically significant lower NO levels were determined in the glaucoma group comparing treatment groups(Bonferroni, P 【0.05). MDA levels were found to be highest in untreated glaucoma group, TAC levels were found to be lower in the glaucoma induction groups than the control group(Bonferroni, P 【0.05).CONCLUSION: Systemic administration of edaravone in experimental glaucoma showed potent neuroprotective activity. The role of oxidative stress causing RGC damage in glaucoma was supported by this study results. 展开更多
关键词 ANTIOXIDANT edaravone GLAUCOMA NEUROPROTECTION
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Edaravone attenuates paraquat-induced lung injury by inhibiting oxidative stress in human type Ⅱalveolar epithelial cells 被引量:8
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作者 Zhi-qiang Cheng Ji-yuan Han +4 位作者 Peng Sun Yu-ying Weng Jiao Chen Guo-yan Wu Hong-xia Ma 《World Journal of Emergency Medicine》 CAS 2012年第1期55-59,共5页
BACKGROUND:Edaravone(3-methyl-1-penyl-2-pyrazolin-5-one) is a potent free-radical scavenger and has the antioxidant ability to inhibit lipid peroxidation.The study aimed to examine the effect of edaravone on protectin... BACKGROUND:Edaravone(3-methyl-1-penyl-2-pyrazolin-5-one) is a potent free-radical scavenger and has the antioxidant ability to inhibit lipid peroxidation.The study aimed to examine the effect of edaravone on protecting the acute injury of human type II alveolar epithelial cells(A549cells) induced by paraquat(PQ) and the change of production of reactive oxygen species(ROS),malondialdehyde(MDA),superoxide dismutase(SOD).METHODS:A549 cells were cultured and divided into PQ group(group P),edaravone-treated group(group E) and normal control group(group C).The cells in group P were exposed to paraquat(600 umol/L),and the cells in group E were treated with edaravone(100 umol/L) additionally,and no drug intervention was given to the cells in group C.Real-time monitoring by LSCM was used to detect the cell response and the intracellular dynamic change of ROS level in A549 cells after administration of PQ and edaravone.And the levels of SOD and MDA were detected respectively by biochemistry colorimetry.Data were expressed as mean ± standard error of the mean.Statistical analysis was carried out with the soft SPSS 16.0.RESULTS:The concentration of intracellular ROS significantly increased when PQ was given to A549 cells.But after administration of edaravone,the concentration of intracellular ROS was decreased.Compared to the PQ group,the levels of SOD in the edaravone group were significantly increased while the levels of MDA were markedly decreased.CONCLUSIONS:Paraquat can increase the oxidative stress,and induce the lipid peroxidation of A549 cells.Edaravone has the effect to scavenge reactive oxygen species,and to protect against the PQ-induced lung toxicity. 展开更多
关键词 PARAQUAT Intracellular reactive oxygen species edaravone A549 cells POISONING
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Edaravone combined with Schwann cell transplantation may repair spinal cord injury in rats 被引量:3
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作者 Shu-quan Zhang Min-fei Wu +4 位作者 Zhe Piao Jin Yao Ji-hai Li Xin-gang Wang Jun Liu 《Neural Regeneration Research》 SCIE CAS CSCD 2015年第2期230-236,共7页
Edaravone has been shown to delay neuronal apoptosis, thereby improving nerve function and the microenvironment after spinal cord injury. Edaravone can provide a favorable environment for theAa:eatment of spinal cord... Edaravone has been shown to delay neuronal apoptosis, thereby improving nerve function and the microenvironment after spinal cord injury. Edaravone can provide a favorable environment for theAa:eatment of spinal cord injury using Schwann cell transplantation. This study used rat models of complete spinal cord transection at T9. Six hours later, Schwann cells were transplanted in the head and tail ends of the injury site. Simultaneously, edaravone was injected through the caudal vein. Eight weeks later, the PKH-26-1abeled Schwann cells had survived and migrated to the center of the spinal cord injury region in rats after combined treatment with edaravone and Schwann cells. Moreover, the number of PKH-26-1abeled Schwann cells in the rat spinal cord was more than that in rats undergoing Schwann cell transplantation alone or rats without any treatment. Horseradish peroxidase retrograde tracing revealed that the number of horserad- ish peroxidase-positive nerve fibers was greater in rats treated with edaravone combined with Schwann cells than in rats with Schwann cell transplantation alone. The results demonstrated that lower extremity motor function and neurophysiological function were better in rats treated with edaravone and Schwann cells than in rats with Schwann cell transplantation only. These data confirmed that Schwann cell transplantation combined with edaravone injection promoted the regeneration of nerve fibers of rats with spinal cord injury and improved neurological function. 展开更多
关键词 nerve regeneration spinal cord injury Schwann cells cell transplantation edaravone motor function electrophysiological function neural regeneration
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Edaravone protects PC12 cells from ischemic-like injury via attenuating the damage to mitochondria 被引量:16
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作者 SONG Ying LI Meng +1 位作者 LI Ji-cheng WEI Er-qing 《Journal of Zhejiang University-Science B(Biomedicine & Biotechnology)》 SCIE CAS CSCD 2006年第9期749-756,共8页
Background: Edaravone had been validated to effectively protect against ischemic injuries. In this study, we investigated the protective effect of edaravone by observing the effects on anti-apoptosis, regulation of B... Background: Edaravone had been validated to effectively protect against ischemic injuries. In this study, we investigated the protective effect of edaravone by observing the effects on anti-apoptosis, regulation of Bcl-2/Bax protein expression and recovering from damage to mitochondria after OGD (oxygen-glucose deprivation)-reperfusion. Methods: Viability of PC 12 cells which were injured at different time of OGD injury, was quantified by measuring MTT (2-(4,5-dimethylthia-zol-2-yl)-2,5-diphenyltetrazolium bromide) staining. In addition, PC 12 cells' viability was also quantified after their preincubation in different concentration of edaravone for 30 min followed by (OGD). Furthermore, apoptotic population of PC 12 cells that reinsulted from OGD-reperfusion with or without preincubation with edaravone was determined by flow cytometer analysis, electron microscope and Hoechst/Pl staining. Finally, change of Bcl-2/Bax protein expression was detected by Western blot. Results: (1) The viability of PC12 cells decreased with time (1-12 h) after OGD. We regarded the model of OGD 2 h, then replacing DMEM (Dulbecco's Modified Eagle's Medium) for another 24 h as an OGD-reperfusion in this research. Furthermore, most PC 12 cells were in the state of apoptosis after OGD-reperfusion. (2) The viability of PC 12 cells preincubated with edaravone at high concentrations (1, 0.1, 0.01 μmol/L) increased significantly with edaravone protecting PC 12 cells from apoptosis after OGD-reperfusion injury. (3) Furthermore, edaravone attenuates the damage of OGD-reperfusion on mitochondria and regulated Bcl-2/Bax protein imbalance expression after OGD-reperfusion. Conclusion: Neuroprotective effects of edaravone on ischemic or other brain injuries may be partly mediated through inhibition of Bcl-2/Bax apoptotic pathways by recovering from the damage of mitochondria. 展开更多
关键词 edaravone lschemia Apoptosis Rat pheochromocytoma (PC 12) cells MITOCHONDRIA Bax Bcl-2 Oxygen-glucose deprivation (OGD)
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Edaravone promotes functional recovery after mechanical peripheral nerve injury 被引量:4
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作者 Teng Zhang Zhengwei Li +3 位作者 Jianli Dong Feng Nan Tao Li Qing Yu 《Neural Regeneration Research》 SCIE CAS CSCD 2014年第18期1709-1715,共7页
Edaravone has been shown to reduce ischemia/reperfusion-induced peripheral nerve injury. However, the therapeutic effect of edaravone on peripheral nerve injury caused by mechanical factors is unknown. In the present ... Edaravone has been shown to reduce ischemia/reperfusion-induced peripheral nerve injury. However, the therapeutic effect of edaravone on peripheral nerve injury caused by mechanical factors is unknown. In the present study, we established a peripheral nerve injury model by crushing the sciatic nerve using hemostatic forceps, and then administered edaravone 3 mg/kg intraperitoneally. The sciatic functional index and superoxide dismutase activity of the sciatic nerve were increased, and the malondialdehyde level was decreased in animals in the edaravone group compared with those in the model group. Bcl-2 expression was increased, but Bax expres- sion was decreased in anterior horn cells of the L4-6 spinal cord segments. These results indicated that edaravone has a neuroprotective effect following peripheral nerve injury caused by mechan- ical factors through alleviating free radical damage to cells and inhibiting lipid peroxidation, as well as regulating apoptosis-related protein expression. 展开更多
关键词 nerve regeneration peripheral nerve injury mechanical injury sciatic nerve injury edaravone lipid peroxidation free radical damage MALONDIALDEHYDE superoxide dismutase Bcl-2 Bax NSFC grant neural regeneration
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Edaravone inhibits apoptosis caused by ischemia/reperfusion injury in a porcine hepatectomy model 被引量:8
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作者 Mitsugi Shimoda Yoshimi Iwasaki +1 位作者 Toshie Okada Keiichi Kubota 《World Journal of Gastroenterology》 SCIE CAS CSCD 2012年第27期3520-3526,共7页
AIM: TO investigate the effect of E3-methyl-l-phe- nyl-2-pyrazolin-5-one (Edr) on hepatic ischemia-reper- fusion (I/R) injury and liver regeneration in a porcine hepatectomy model. METHODS: One hour ischemia was... AIM: TO investigate the effect of E3-methyl-l-phe- nyl-2-pyrazolin-5-one (Edr) on hepatic ischemia-reper- fusion (I/R) injury and liver regeneration in a porcine hepatectomy model. METHODS: One hour ischemia was induced by occlud- ing the vessels and the bile duct of the right and median lobes. A 40% left hepatectomy was performed after re- perfusion. Six animals received Edr (3 mg/kg per hour) intravenously and six control animals received saline just before reperfusion. Remnant liver volume, hemody- namics, aspartate aminotransferase (AST), alanine ami- notransferase, lactate dehydrogenase and lactic acid, were compared between the groups. The expression of transforming growth factor-β (TGF-β1) and toll-like receptor (TRL) mRNA in hepatic tissues was examined using reverse transcription polymerase chain reaction. Apoptosis was demonstrated by terminal deoxynucleo- tidyl transferase dUTP nick end labeling (TUNEL) stain- ing, respectively. RESULTS: Serum AS-I- (P = 0.029), and toll like recep- tor 4 level (P = 0.043) were significantly lower after 3 hin animals receiving Edr. In addition, TUNEL staining in Edr-treated pigs showed significantly fewer hepatocytes undergoing apoptosis compared with control pigs. After 1 mo, all factors were non-significantly different between the two groups. CONCLUSION: Edr is considered to reduce hepatic injury in the early stage of I/R injury in a porcine model. 展开更多
关键词 edaravone Ischemia-reperfusion injury Liver resection Transforming growth factor-13 Toll likereceptor 4
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Protective effects of edaravone on diffuse brain njury in rats 被引量:3
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作者 Jian-min Li Pan Zhang +2 位作者 Ya-ning Zhao Chang-xiang Chen Shu-xing Li 《World Journal of Emergency Medicine》 SCIE CAS 2011年第3期222-227,共6页
BACKGROUND:Edaravone can alleviate brain injury and improve neurological functions and symptoms. This study aimed to investigate the effect of edaravone on the p38Mitogen-activated protein kinases/Caspase-3 (p38MAPK... BACKGROUND:Edaravone can alleviate brain injury and improve neurological functions and symptoms. This study aimed to investigate the effect of edaravone on the p38Mitogen-activated protein kinases/Caspase-3 (p38MAPK/Caspase-3) pathway after diffuse brain injury (DBI) in rats. METHODS: DBI models were established according to the description of Marmarou's method. A total of 250 rats were divided (random number) into four groups: control group (CG, n=45), model group (MG, n=77), low-dose edaravone group (n=67, dosage 5 mg/kg) and high-dose edaravone group (n=61, dosage 10 mg/kg). After 1,6, 24, 48, and 72 hours after injury, brain tissues were collected. The changes of neuron morphous in the hippocampal region were observed through Nissl staining. The expression levels of phosphorylated p38MAPK and caspase-3 were detected by immunohistochemistry and Western blotting respectively. Learning and memory function were tested with Morris water maze from the 3rd to 7th day after injury. RESULTS: Some neurons had histopathologic changes of necrosis and apoptosis in the model group compared with the control group. The phosphorylated p38MAPK expressions increased at 1,6, 4, and 48 hours (P〈0.05), but no significant difference was observed at 72 hours (0.54±0.19 vs. 0.40±0.14, P〉0.05). Caspase-3 expressions increased at 6, 24, 48, and 72 hours respectively (P〈0.05), but there was no significant difference at 1 hour (0.59±0.29 vs. 0.40±0.17, P〉0.05). From the 3rd to 6th day during the Morris water maze test, the latency to find the platform was significantly prolonged (P〈0.05) and times of rats crossing the platform was decreased on the 7th day (2.28±1.18 vs. 8.20±1.52, P〈0.05). The phosphorylated p38MAPK expressions decreased at 6, 24 and 48 hours respectively in the low dose edaravone group compared with the model group (P〈0.05), whereas no significant difference was seen at 1 hour (1.66±0.80 vs. 1.85±0.86, P〉0.05). Caspase-3 expression decreased at 6, 24, 48, and 72 hours (P〈0.05). The latency to find the platform was significantly shortened (P〈0.05), and times of rats crossing the platform increased (4.17±1.15 vs. 2.28±1.18, P〈0.05). The above mentioned parameters changed more significantly in the high-dose edaravone group than in the low-dose edaravone group. CONCLUSION:Edaravone can alleviate brain tissue damage after DBI, inhibit p38MAP signal activation after early injury, reduce the expression of caspase-3, and promote the recovery of neurological function in the late period. 展开更多
关键词 Diffuse brain injury Mitogen-activated protein kinases CASPASE-3 Learning-memory edaravone
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Neuroprotective role of edaravone and the effects of endoplasmic reticulum stress in an adult rat model of focal cerebral ischemia/reperfusion 被引量:2
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作者 Xiangmin Shen Liming Tan +6 位作者 Yunhai Liu Hainan Zhang Chunyu Wang Qidong Yang QingHuang Lin Zhou Zhenyu Tang 《Neural Regeneration Research》 SCIE CAS CSCD 2010年第3期197-204,共8页
BACKGROUND: Endoplasmic reticulum (ER) stress impairs ER functions and leads to the accumulation of unfolded or misfolded proteins in the ER lumen. ER stress-induced cell death plays an important role in cerebral i... BACKGROUND: Endoplasmic reticulum (ER) stress impairs ER functions and leads to the accumulation of unfolded or misfolded proteins in the ER lumen. ER stress-induced cell death plays an important role in cerebral ischemia. Edaravon (3-methyl-1-phenyl-2-pyrazolin-5-one) is a potent and novel scavenger of free radicals that inhibit delayed neuronal death, as demonstrated by in vitro and animal studies. However, its effect on ER stress and induced neuronal apoptosis in a rat model of brief middle cerebral artery occlusion remains unclear. OBJECTIVE: To explore the effects of edaravone on the expression of ER stress-related factors and neuronal apoptosis, based on the hypothesis that edaravone influences ER stress in a rat model of cerebral ischemia/reperfusion. DESIGN, TIME AND SETTING: A randomized, controlled, animal study was performed at the Laboratory of Department of Neurology, Xiangya Hospital and the Department of Laboratory Animals, Xiangya Medical College, Central South University in China from June 2005 to May 2006. MATERIALS: Edaravone was purchased from Simcere Pharmaceutical Group, China. METHODS: A total of 216 adult, male, Sprague Dawley rats were randomly assigned to sham-surgery, model and edaravone groups, with 72 rats in each group, Brief middle cerebral artery occlusion was established in the model and edaravone groups. In addition, the edaravone group rats were injected with 3 mg/kg edaravone through the tail vein. MAIN OUTCOME MEASURES: RNA-dependent protein kinase-like endoplasmic reticulum eukaryotic translation initiation factor 2a kinase (PERK) and C/EBP homology protein (CHOP) mRNA expression in the ischemic parietal cortex was determined by reverse transcriptionpolymerase chain reaction; phosphorylated PERK and CHOP protein expression was detected by immunohistochemistry; neuronal apoptosis was detected by TdT-mediated-dUTP nick end labeling. RESULTS: Neurological deficit scores were significantly reduced in the edaravone group compared to the model group at 12, 24, and 72 hours following reperfusion (P〈 0.05). In addition, PERK and CHOP mRNA as well as phosphorylated PERK and CHOP protein expression were significantly reduced in the edaravone group compared to the model group at 1,3, and 6 hours following reperfusion (P 〈 0.05, P 〈 0.01). CHOP mRNA expression was decreased in the edaravone group compared to the model group at 3, 6, 12, and 24 hours following reperfusion (P〈 0.01), while CHOP protein expression was less than the model group at 6, 12, and 24 hours following reperfusion (P 〈 0.05). CONCLUSION: Edaravone treatment resulted in decreased PERK and CHOP expression following ischemia/reperfusion, as well as reduced neuronal apoptosis. Edaravone exhibited a neuroprotective role by inhibiting endoplasmic reticulum stress. 展开更多
关键词 edaravone cerebral ischemia/reperfusion endoplasmic reticulum stress RNA-dependent protein kinase-like endoplasmic reticulum elF2a kinase C/EBP homology protein brain injury neural regeneration
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Edaravone protects against oxygen-glucose-serum deprivation/restoration-induced apoptosis in spinal cord astrocytes by inhibiting integrated stress response 被引量:2
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作者 Bin Dai Ting Yan +7 位作者 Yi-xing Shen You-jia Xu Hai-bin Shen Dong Chen Jin-rong Wang Shuang-hua He Qi-rong Dong Ai-liang Zhang 《Neural Regeneration Research》 SCIE CAS CSCD 2017年第2期283-289,共7页
We previously found that oxygen-glucose-serum deprivation/restoration(OGSD/R) induces apoptosis of spinal cord astrocytes, possibly via caspase-12 and the integrated stress response, which involves protein kinase R-... We previously found that oxygen-glucose-serum deprivation/restoration(OGSD/R) induces apoptosis of spinal cord astrocytes, possibly via caspase-12 and the integrated stress response, which involves protein kinase R-like endoplasmic reticulum kinase(PERK), eukaryotic initiation factor 2-alpha(eIF2α) and activating transcription factor 4(ATF4). We hypothesized that edaravone, a low molecular weight, lipophilic free radical scavenger, would reduce OGSD/R-induced apoptosis of spinal cord astrocytes. To test this, we established primary cultures of rat astrocytes, and exposed them to 8 hours/6 hours of OGSD/R with or without edaravone(0.1, 1, 10, 100 μM) treatment. We found that 100 μM of edaravone significantly suppressed astrocyte apoptosis and inhibited the release of reactive oxygen species. It also inhibited the activation of caspase-12 and caspase-3, and reduced the expression of homologous CCAAT/enhancer binding protein, phosphorylated(p)-PERK, p-eIF2α, and ATF4. These results point to a new use of an established drug in the prevention of OGSD/R-mediated spinal cord astrocyte apoptosis via the integrated stress response. 展开更多
关键词 nerve regeneration edaravone apoptosis astrocytes integrated stress response reactive oxygen species PERK eIF2α activating transcription factor 4 CCAAT/enhancer binding protein homologous protein caspase-3 caspase-12 neural regeneration
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Edaravone Enhances the Viability of Ischemia/reperfusion Flaps 被引量:1
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作者 张栋益 康深松 +1 位作者 张正文 吴蕊 《Journal of Huazhong University of Science and Technology(Medical Sciences)》 SCIE CAS 2017年第1期51-56,共6页
The purpose of the experiment was to study the efficacy of edaravone in enhancing flap viability after ischemia/reperfusion(IR) and its mechanism. Forty-eight adult male SD rats were randomly divided into 3 groups:... The purpose of the experiment was to study the efficacy of edaravone in enhancing flap viability after ischemia/reperfusion(IR) and its mechanism. Forty-eight adult male SD rats were randomly divided into 3 groups: control group(n=16), IR group(n=16), and edaravone-treated IR group(n=16). An island flap at left lower abdomen(6.0 cm×3.0 cm in size), fed by the superficial epigastric artery and vein, was created in each rat of all the three groups. The arterial blood flow of flaps in IR group and edaravone-treated IR group was blocked for 10 h, and then the blood perfusion was restored. From 15 min before reperfusion, rats in the edaravone-treated IR group were intraperitoneally injected with edaravone(10 mg/kg), once every 12 h, for 3 days. Rats in the IR group and control group were intraperitoneally injected with saline, with the same method and frequency as the rats in the edaravone-treated IR group. In IR group and edaravone-treated IR group, samples of flaps were harvested after reperfusion of the flaps for 24 h. In the control group, samples of flaps were harvested 34 h after creation of the flaps. The content of malondialdehyde(MDA) and activity of superoxide dismutase(SOD) were determined, and changes in organizational structure and infiltration of inflammatory cells were observed by hematoxylin-eosin(HE) staining, apoptotic cells of vascular wall were marked by terminal deoxynucleotidyl transferase-mediated d UTP nick-end labeling(TUNEL) assay, and the apoptotic rate of cells in vascular wall was calculated. The ultrastructural changes of vascular endothelial cells were observed by transmission electron microscopy(TEM). Seven days after the operation, we calculated the flap viability of each group, and marked vessels of flaps by immunohistochemical staining for calculating the average number of subcutaneous vessels. The results showed that the content of MDA, the number of multicore inflammatory cells and apoptotic rate of cells in vascular wall in the edaravone-treated IR group were significantly lower than those in the IR group. The activity of SOD, flap viability and average number of subcutaneous vessels in the edaravone-treated IR group were significantly higher than those in the IR group. All the differences were statistically significant. The ultrastructure injury of vascular endothelial cells in the edaravone-treated IR group was slighter than that in IR group. It was concluded that edaravone can significantly enhance IR flap viability and protect flap vessels, which is related to scavenging oxygen free radicals, reducing the consumption of SOD, reducing the extent of lipid peroxidation and inflammation, and protecting functional structure of vessels in the early stages of reperfusion. 展开更多
关键词 free radical scavengers edaravone ischemia/reperfusion injury skin flap
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