胶质原纤维酸性蛋白

胶质原纤维酸性蛋白的相关文献在2000年到2022年内共计107篇,主要集中在神经病学与精神病学、基础医学、中国医学 等领域,其中期刊论文105篇、会议论文1篇、专利文献362083篇;相关期刊78种,包括中国组织化学与细胞化学杂志、解剖学杂志、中国康复理论与实践等; 相关会议1种,包括2012年全国有毒中药的研究及其合理应用交流研讨会等;胶质原纤维酸性蛋白的相关文献由407位作者贡献,包括饶志仁、刘庆莹、朱长庚等。

胶质原纤维酸性蛋白—发文量

期刊论文>

论文:105 占比:0.03%

会议论文>

论文:1 占比:0.00%

专利文献>

论文:362083 占比:99.97%

总计:362189篇

胶质原纤维酸性蛋白—发文趋势图

胶质原纤维酸性蛋白

-研究学者

  • 饶志仁
  • 刘庆莹
  • 朱长庚
  • 张平
  • 张辉
  • 王伟
  • 刘宝军
  • 刘洪臣
  • 刘雪梅
  • 华田苗
  • 期刊论文
  • 会议论文
  • 专利文献

搜索

排序:

年份

    • 田园; 韩若东; 赵江明
    • 摘要: 目的 研究氧化苦参碱对急性脑梗死大鼠的脑保护作用及脑组织胶质原纤维酸性蛋白(GFAP)、生长相关蛋白-43(GAP-43)表达的影响.方法 采用线栓法制备急性脑梗死大鼠模型,将成功建立的急性脑梗死大鼠随机分为模型组(n=18)与实验组(n=18);假手术组(n=18)仅分离动脉,不结扎插线.实验组大鼠腹腔注射氧化苦参碱120 mg·kg-1·d-1,假手术组与模型组腹腔注射等量生理盐水,每天1次,连续干预5 d.采用干湿法测定各组大鼠干预1,3,5 d的脑组织含水量;用苏木精-伊红(HE)染色观察脑组织病理学特点;用酶联免疫吸附(ELISA)法检测血清白细胞介素-2(IL-2)、肿瘤坏死因子-α(TNF-α)与白细胞介素-8(IL-8)水平;用蛋白质印迹(Wb)法检测脑组织GFAP、GAP-43蛋白的表达水平.结果 假手术组、模型组与实验组大鼠干预5 d时的脑组织含水量分别为(48.32±0.22)%,(89.73±0.31)%,(64.27±0.24)%;脑组织GFAP蛋白相对表达量分别为0.47±0.10,0.96±0.04,0.75±0.13;GAP-43蛋白相对表达量分别为0.68±0.12,0.14±0.06,0.32±0.10.干预1,3,5 d,与假手术组比较,模型组同一时间点脑组织含水量均显著增多,且以干预3 d时达到最高峰;与模型组比较,实验组同一时间点脑组织含水量显著减少,且以干预5 d时最少;与假手术组比较,模型组大鼠血清IL-2、IL-8与TNF-α水平及脑组织GFAP蛋白相对表达量均显著升高,实验组低于模型组;而模型组大鼠脑组织GAP-43蛋白相对表达量显著低于假手术组,实验组高于模型组(均P<0.05).结论 氧化苦参碱可显著缓解急性脑梗死大鼠脑水肿,抑制炎症反应,同时可显著抑制脑组织GFAP蛋白表达,促进GAP-43蛋白表达,从而发挥脑保护作用.
    • 吴嶛; 孙颖; 孙波; 倪小宇; 徐欣; 左鹏; 倪贵华
    • 摘要: 目的 观察辛醇对大鼠脑缺血再灌注后星形胶质细胞及胶质原纤维酸性蛋白(GFAP) 表达的影响,探讨辛醇脑保护的可能机制.方法 取48只健康成年雄性SD大鼠,随机分为假手术组、模型组、溶剂对照组和辛醇干预组,每组12只.假手术组不造模,其余3组采用线栓法制作大鼠大脑中动脉缺血再灌注损伤模型,缺血时间为2 h,再灌注时间为24 h.辛醇干预组于缺血前30 min按5 mmol /kg体质量腹腔注射辛醇溶液,溶剂对照组于缺血前30 min腹腔注射等容积5% 二甲基亚砜溶液,假手术组及模型组于同时腹腔注射等容积0.9%氯化钠注射液.各组大鼠处死前均进行神经功能缺损评分; 尼氏染色法观察神经细胞损伤情况; 免疫组织化学及蛋白质印迹法检测缺血半暗带GFAP的表达.结果 缺血再灌注24 h后,模型组神经功能缺损评分明显高于假手术组[(2.8 ± 0.4) 分比0分](P 0.05); 辛醇干预组神经功能缺损评分[(1.1 ± 0.4) 分]明显低于模型组(P 0.05) .辛醇干预组缺血半暗带GFAP阳性细胞数明显少于模型组(P 0.05); the score in octanol group[(1.1 ± 0.4) ] was significantly lower than that in model group(P 0.05). The number of GFAP-positive cells in octanol group was significantly less than that in model group (P < 0.05). After reperfusion(24 h) ,expression of GFAP protein decreased in sham operation group and increased in model group; there was no significant difference between solvent control group and model group; expression of GFAP protein in octanol group was significantly lower than that in model group. Conclusion Octanol can inhibit the activation of astrocytes and protect brain against ischemia-reperfusion injury.
    • 卢关伊; 庞冲; 陈文强; 陈瑛; 吴宁; 李锦
    • 摘要: 目的 研究水通道蛋白4(AQP4)在神经病理性疼痛中的作用,并探讨其与脊髓星形胶质细胞激活和促炎细胞因子释放的关系.方法 应用AQP4基因敲除(KO)和野生型(WT)小鼠建立坐骨神经分支损伤模型(SNI),观察AQP4基因敲除对疼痛行为的影响,随后采用Western印迹法(WB)检测SNI模型小鼠脊髓中星形胶质细胞激活相关标志物胶质原纤维酸性蛋白(GFAP)表达的变化,采用ELISA法检测SNI模型小鼠脊髓中促炎细胞因子(TNF-α、IL-6)含量的变化.结果 SNI手术后,与WT组相比,KO组小鼠的机械刺激痛觉超敏程度显著降低(P<0.01),而经假手术(Sham)处理的WT与KO组小鼠无差异(P>0.05),提示AQP4基因敲除可减轻神经病理性疼痛.WB结果显示,后术14d,与WT-Sham组相比,WT-SNI组小鼠脊髓GFAP含量显著高升高(P<0.01);与WT-SNI组相比,KO-SNI组小鼠脊髓GFAP含量显著降低(P<0.01),提示AQP4基因敲除抑制了小鼠SNI模型脊髓星形胶质细胞的激活.ELISA结果显示,术后14d,与WT-Sham组相比,WT-SNI组小鼠脊髓促炎细胞因子TNF-α和IL-6含量均显著升高(P<0.05,P<0.01);与WT-SNI组相比,KO-SNI组小鼠脊髓TNF-α和IL-6的含量均显著降低(P<0.05,P<0.01),提示AQP4基因敲除可降低小鼠SNI模型脊髓促炎细胞因子水平.结论 AQP4基因敲除可能通过降低脊髓中星形胶质细胞的激活和促炎细胞因子的生成而减轻神经病理性疼痛.
    • 刘先岭; 王培山; 智明明; 王静静; 陈辰
    • 摘要: 目的 探讨脉冲射频对神经源性疼痛(NP)大鼠脊髓胶质原纤维酸性蛋白(GFAP)、蛋白激酶C-α1相互作用蛋白(PICK1)水平的影响.方法 150只雄性成年SD大鼠随机分为假性手术组、模型组、脉冲射频2 Hz组、4 Hz组、8 Hz组,每组30只.分别于术前、术后1、3、7、14 d记录各组大鼠热缩腿反射潜伏期(TWL)、机械缩足反射阈值(MWT),抽取各组大鼠脊髓应用Western印迹法测定各组脊髓中GFAP蛋白、PICK1蛋白水平.结果 模型组、2 Hz组、4 Hz组、8 Hz组术后1、3、7、14 d TWL、MWT水平显著短于假性手术组(P<0.05),模型组显著短于射频2 Hz组、4 Hz组、8 Hz组(P<0.05);随着射频频率增加,TWL、MWT水平显著升高(P<0.05),模型组、射频2 Hz组、4 Hz组、8 Hz组脊髓术后1、3、7、14 d GFAP、PICK1表达水平显著高于假性手术组(P<0.05),模型组高于射频2 Hz组、4 Hz组、8 Hz组(P<0.05);而射频组中随着作用频率的增加,脊髓GFAP蛋白、PICK1蛋白表达水平显著下降(P<0.05).结论 脉冲射频能有效减轻坐骨神经压迫性损伤所致NP大鼠热和机械性痛觉过敏,能有效抑制脊髓GFAP、PICK1表达;随着射频频率的增加,效果越理想,射频对NP有治疗效果.
    • 张瑶; 张星慧; 李美香; 张弛; 贺鹏程; 蒋湘; 尹卫东; Moshe Laudon; 石金凤
    • 摘要: 目的 探讨Neu-P11对急性高眼压大鼠眼压及视网膜胶质原纤维酸性蛋白(glial fibrillary acid protein,GFAP)表达的影响.方法 24只雄性SD大鼠随机分为:正常对照组、高眼压组、褪黑素治疗组和Neu-P11治疗组,每组6只,后3组采用Trendelenburg卧位法建立高眼压模型,各组通过眼角膜滴注方法给药.正常对照组和高眼压组滴注10 μL生理盐水,褪黑素治疗组和Neu-P11治疗组分别滴注10 μL 100 μmol·L-1褪黑素和NeuP11药物治疗,给药后休息2h,再次置于卧位45 min后每小时测1次眼压,共6次,观察1周,重复实验1次.实验末注射过量戊巴比妥钠处死大鼠,留取各组大鼠眼球常规组织学切片观察SD大鼠视网膜形态学变化;免疫组织化学染色观察视网膜GFAP的表达.结果 正常对照组眼压为(13.61±0.55) mmHg(1 kPa=7.5 mmHg),高眼压组眼压为(41.26±1.73)mmHg(P <0.01),即急性高眼压大鼠模型建立成功.与正常对照组相比,高眼压组大鼠视网膜水肿增厚,层次不清晰,GFAP表达呈强阳性.而褪黑素治疗组和Neu-P11治疗组大鼠眼压较高眼压组显著降低,GFAP蛋白阳性表达明显减弱.结论 Neu-P11能够降低急性高眼压大鼠眼压,抑制视网膜组织胶质细胞的激活,降低GFAP表达,保护视网膜.%Objective To explore the effects of the new melatonin nonselective agonists Neu-P11 on intraocular pressure (IOP) and glial fibrillary acid protein (GFAP) expression in the retina of acute high IOP rat.Methods Twenty-four male Sprague-Dawley rats were randomly divided into 4 groups (6 cases in each group):Normal IOP with local treatment (NIL) group,high IOP with local treatment (HIL) group,HILwith melatonin treatment (HIL-M) group,HIL with Neu-P11 treatment (HIL-N) group.10 μL normal saline was instilled in NIL group and HIL group,while 10 μL 100 μmol · L-1 Mel/Neu-P11 treated in HIL-M group and HIL-N group.After 2 hours of rest,rats were placed in the Trendelenburg position duration 45 minutes.And then,IOP was measured every hour for 6 hours,and repeated it for a week.The excessive sodium pentobarbital was injected to SD rats at the end of the experiment.The rat eyeballs were took out to perform HE and immunohistochemical staining to detect retina GFAP protein expression.Results After a week,IOP in HIL group was (41.26 ± 1.73) mmHg (1 kPa =7.5 mmHg),NIL group was (13.61 ± 0.55) mmHg,which mean the Trendelenburg could induce high IOP in SD rats.Compared with the NIL group,the retinal becoming thick,the level of organization was not clear and the expression of GFAP protein was quite high in HIL group.At the same time,the GFAP protein expression and IOP were significantly weakened in HIL-M group and HIL-N group compared with HIL group.Conclusion Neu-P1 1 can reduce IOP,inhibit the activation of gliocyte,and decrease the expression of GFAP to protect the retina.
    • 吴敏; 方庆; 师忠芳; 徐立新; 董丽萍; 闫旭; 杨少华; 袁芳
    • 摘要: Objective To investigate the protective effect of methylene blue (MB) on blood-brain barrier (BBB) injury after focal cere-bral ischemia-reperfusion in rats. Methods 18 male Sprague-Dawley rats were randomly divided into sham-operated group (n=6), model group (n=6) and MB treatment group (n=6). The left middle cerebral arteries were occluded for 1 hour and reperfused. MB was infused intra-venously immediately after reperfusion (3 mg/kg) and again 2 hours post-reperfusion (1.5 mg/kg), while normal saline was administered in the model group. The sham-operated group was treated as same as the model group without occlusion and infusion. HE staining was used to observe the histological injury in the cortex around the infarcted region 47 hours after reperfusion, while albumin immunohistochemistry was used to evaluate the permeability of the BBB, and immunohistochemistry and double immunofluorescence staining were used to exam-ine the expressions of glial fibrillary acidic protein (GFAP) and aquaporin-4 (AQP-4). Results HE staining showed that cells and blood ves-sels were not intact in the cortex around the infarcted region in the model group and they were better in the MB treatment group. The expres-sions of the albumin, GFAP and AQP-4 were higher in the model group than in the sham-operated group (P<0.01), and were lower in MB treatment group than in the model group (P<0.05). The double immunofluorescence staining showed the colocalization of GFAP and AQP-4 in the astrocytes. Conclusion MB may ameliorate the BBB disruption induced by focal cerebral ischemia-reperfusion through reducing glio-cyte proliferation and down-regulation of AQP-4 expression in rats.%目的探讨亚甲基蓝对大鼠局灶性脑缺血再灌注引起血脑屏障破坏的保护作用。方法雄性Sprague-Dawley大鼠18只随机分为假手术组(n=6)、模型组(n=6)和亚甲基蓝组(n=6)。用线栓法制备大鼠左侧大脑中动脉栓塞1 h再灌注模型。亚甲基蓝组于再灌注即刻及再灌注2 h分别静脉给予亚甲基蓝3 mg/kg、1.5 mg/kg;模型组给予相同体积的生理盐水;假手术组手术操作与模型组相同,不插入线栓,不静脉注射药物。再灌注47 h后HE染色观察大鼠脑缺血周边皮层组织学结构,白蛋白免疫组化染色法检测血脑屏障通透性的变化,免疫组化染色法和免疫荧光双标染色法检测胶质原纤维酸性蛋白(GFAP)和水通道蛋白-4(AQP-4)的表达。结果 HE染色显示,模型组缺血周边大脑皮层的细胞和血管形态不完整,而亚甲基蓝组病理变化减轻;模型组白蛋白、GFAP和AQP-4表达均明显高于假手术组(P<0.01),亚甲基蓝组白蛋白、GFAP、AQP-4表达均低于模型组(P<0.05)。免疫荧光双标染色显示,AQP-4与GFAP在星形胶质细胞上共定位。结论亚甲基蓝可能是通过减轻胶质细胞增生及下调AQP-4表达来改善局灶性脑缺血再灌注损伤引起的血脑屏障破坏。
    • 师思; 王晓良
    • 摘要: Diabetes mellitus can cause central nervous system disorder that is summarized as diabetic encephalopathy, which manifests in cognitive dysfunction and other mental illnesses. Astrocyte ,with a huge number and extensive functions,is an im⁃portant part of the central nervous system. Morphological and functional changes in astrocyte have been observed in diabetes mellitus , which involve the quantity,the expression of neurotransmitters and relative transporters,the activity of enzyme,the storage of glyco⁃gen and the intercellular connection and communication.%糖尿病可引起中枢神经系统病变,功能上表现为学习和记忆能力的减退,病理学证实脑内结构和功能改变,即糖尿病脑病。星形胶质细胞是中枢神经系统的重要组成部分,数量庞大且功能广泛。现已发现,在糖尿病的早期,脑内星形胶质细胞就已发生改变,表现为细胞体积和数量的变化,随后相继发生糖原、能量供应、递质转运体和酶活性、以及炎症介质和神经营养因子释放的改变,对糖尿病脑病的发生可能有重要作用。
    • 孙熠; 陈泊霖; 金学隆
    • 摘要: Objective To observe the dynamic changes of capillary permeability and the expression of glial fibrillary acid protein (GFAP)in cerebral cortex after radiation-induced brain injury (RIBI)in rats.Methods Forty-eight adult male healthy SD rats were randomly divided into groups A,B,C and the control group,12 in each.RIBI models of groups A,B and C were established by CT scanning with a whole dose of 6 Gy,2 Gy/time for 3 times.Animals in the control group were subjected to the same surgical procedure without cranial irradiation.The expression of GFAP in the parietal cor-tex was analyzed at different time points (7,14 and 28 h)by immunohistochemistry (IHC),and the capillary permeability was evaluated by microscope vascular camera device and microcirculation video recording system.Results The capillary permeability in the groups A,B and C was 0.70 ±0.082,0.58 ±0.019,0.54 ±0.058 and 0.39 ±0.073,which was sig-nificantly higher than that in the control group (0.39 ±0.073)(all P<0.05).Similarly,IHC indicated that the expres-sion levels of GFAP in the groups A,B,C were 145 006 ±5 266.8,101 250 ±9 034.8 and 68 313 ±7 633.4,which were significantly higher as compared with that of the control group (17 617 ±5 870.7),(all P<0.05).Conclusion The level of GFAP is high in the brain cortex of RIBI rats,which is consistent with the change of capillary permeability after RI-BI,and this strongly indicates that GFAP may participate the occurrence and development of RIBI.%目的:观察放射性脑损伤(RIBI)大鼠脑皮层胶质原纤维酸性蛋白(GFAP)及微血管通透性。方法SPF 清洁级成年健康雄性SD 大鼠48只分为A、B、C组和对照组各12只。A、B、C组采用CT大脑局部照射造成RIBI,2 Gy/次,共照射3次,总照射剂量6 Gy。对照组仅腹腔注射麻醉大鼠,不行大脑局部照射。分别于照射7、14、28 d时取各组部分大鼠,断头处死后取脑组织,采用免疫组化法检测各组脑皮层GFAP。于照射7、14、28 d时取各组部分大鼠,断头处死后取脑组织,采用微循环显微仪观察各组损伤脑皮层微血管通透性。结果 A、B、C组和对照组的血管通透性分别为0.70±0.082、0.58±0.019、0.54±0.058、0.39±0.073,组间比较,P均<0.05。A、B、C组和对照组脑皮层 GFAP的 IOD值分别为145006±5266.8、101250±9034.8、68313±7633.4、17617±5870.7,组间比较,P均<0.05。结论 RIBI大鼠损伤脑皮层存在GFAP高表达,GFAP的表达水平与微血管通透性的变化趋势相一致,GFAP可能参与了RIBI的发生发展。
  • 查看更多

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号