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1.
为探讨周围支切断对DRG神经元BDNF ,NT 3及其mRNA表达的影响 ,将 5只成年猫麻醉后暴露双侧L7DRG ,于一侧距DRG 1cm处切断外周支 ,另一侧为对照。动物存活 3d后取两侧L7DRG制作 2 0 μm厚冷冻切片。分别用BDNF、NT 3抗体及BDNFcRNA ,NT 3cRNA探针 (地高辛末端标记 )行ABC免疫组化和原位杂交染色。观察BDNF ,NT 3及其mRNA的阳性产物部位 ,计数恒定面积内BDNF ,NT 3及其mRNA的阳性神经元数量。结果BDNF及mRNA的阳性细胞主要是DRG胞体偏小的神经元 (135 7μm)。而NT 3及mRNA的阳性细胞则主要是胞体偏大的神经元 (5 710 0 μm)。恒定面积内BDNF及其mRNA和NT 3及其mRNA的阳性神经元数量实验侧分别是 16.4± 0 .7,11.1± 1.4和 2 4 .5± 2 .1,2 2 .8± 3.2 ,而对照侧则分别是 10 .3± 1.9,6.1± 0 .9和 12 .5± 2 .7,15 .3± 4 .1。比较两侧BDNF、NT 3及其mRNA的阳性神经元数量均有显著差异 (P <0 .0 5 )。表明周围支切断可致DRGBDNF ,NT 3的表达明显增多。提示BDNF ,NT 3可能在外周神经切断的早期反应中发挥作用  相似文献   

2.
百草枯对小鼠黑质多巴胺能神经元的选择性损害   总被引:2,自引:2,他引:0  
目的:探讨百草枯对黑质部多巴胺能神经元的损害是否具有选择性。方法:用口服百草枯的途径,建立小鼠帕金森病模型;应用原位杂交技术观察DAT和VMAT2在不同脑区的mRNA表达水平并测定两者的比值,采用细胞计数观察百草枯干预后多巴胺能神经元的损害。结果:在黑质部DATmRNA和VMAT2mRNA的比值最高;在红核和下丘脑室旁核区域DATmRNA与VMAT2mRNA的比值和黑质部相比较低(P<0·01)。百草枯干预后黑质部的多巴胺能神经元减少37·7%;红核和下丘脑室旁核区的多巴胺能神经元分别减少12·2%和13·1%。结论:百草枯对黑质部多巴胺能神经元的损害具有相对选择性,其原因可能与黑质部DATmRNA和VMAT2mRNA的比值高有关。  相似文献   

3.
SMN蛋白是SMA致病基因的产物。SMN蛋白是稳定的多蛋白复合体———SMN蛋白复合体的一部分,此复合体可见于细胞质和核gems小体内。SMN复合体中除了SMN蛋白外,至少包括六种其他的蛋白,分别命名为Gemins2~7。SMN复合体和很多蛋白及RNPs(snRNPs和snoRNPs)中的成分相互作用,从而介导了Sm核心域的形成、参与mRNA和rRNA的代谢,还可能参与了细胞凋亡过程。  相似文献   

4.
目的研究水通道蛋白-4(aquaporin4,AQP4)在缺血性脑损伤大鼠脑内的表达,及丝裂原活化蛋白激酶(MAPKs)信号转导通路抑制剂U0126对其表达的影响。方法用线栓法建立缺血性脑损伤大鼠模型,测定脑组织含水量及伊文斯蓝含量,并采用免疫组织化学、Westernblot和逆转录-聚合酶链反应技术,检测AQP4的表达。测定预先经侧脑室给予U0126后MAPKs信号通路关键蛋白ERK1/2和ELK1磷酸化水平,同时观察U0126对脑水肿和AQP4表达的影响。结果正常组AQP4表达较低[蛋白(吸光度值,下同):123·1±1·0,mRNA(吸光度比值,下同):0·173±0·017],在缺血损伤后表达升高(蛋白:153·6±0·8,mRNA:0·400±0·015),脑组织含水量及伊文斯蓝含量增加,给予U0126后AQP4的表达和脑组织含水量降低(蛋白:149·0±1·1,mRNA:0·328±0·010,P<0·01),同时ERK1/2和ELK1磷酸化水平降低。结论缺血性损伤后AQP4表达上升,脑水肿明显,预先给予U0126可抑制AQP4的表达,减轻脑水肿。  相似文献   

5.
Aβ_(1-40)海马注射对大鼠脑内一氧化氮合酶表达的影响   总被引:6,自引:0,他引:6  
目的 探讨一氧化氮合酶 (NOS)在 β淀粉样蛋白 (Aβ)神经毒性及阿尔茨海默病 (AD)病理机制中的作用。方法 应用免疫组化方法 ,观察大鼠海马齿状回Aβ1 4 0 注射后神经元型一氧化氮合酶 (nNOS)和诱导型一氧化氮合酶 (iNOS)表达变化。结果 正常大鼠海马齿状回区含nNOS神经元计数为 8 96± 0 35个 /视野 ;生理盐水注射后局部含nNOS神经元无明显变化 (8 97± 0 2 9个 /视野 ) ;Aβ1 4 0 注射后 ,注射区周围含nNOS神经元数目显著减少 (2 98± 0 2 4个 /视野 )。正常及生理盐水注射组脑内未见iNOS表达 ;Aβ1 4 0 注射后 2d、10d和 30d ,注射区持续出现大量含iNOS的胶质细胞 (主要为星形胶质细胞 ) ,反应面积分别为 0 90 5± 0 0 82、0 96 2± 0 16 1、0 935± 0 12 5mm2 。结论 Aβ1 4 0 海马注射可损伤局部含nNOS神经元及诱导胶质细胞iNOS表达 ,NOS在Aβ神经毒性和AD发病中有重要作用。  相似文献   

6.
目的 检测体外人骨髓间充质干细胞(human mesenchymal stem cells,hMSCs)经DMSO/BHA联合诱导后所分化的神经元样细胞表达单胺类受体基因的状况,以探讨体外诱导hMSCs向神经元样细胞分化的条件和机制.方法 采用密度梯度离心法和贴壁培养的方法分离纯化hMSCs,DMSO/BHA联合诱导分化,免疫细胞化学法检测神经元特异性烯醇化酶(neurone specific enolase,NSE)的表达,RT-PCR检测5-HT2受体和多巴胺2受体(DRD2)mRNA.结果 分离纯化的hMSCs加入诱导剂后,hMSCs形成多极神经元的形态;免疫组化结果显示NSE蛋白表达阳性;RT-PCR结果显示诱导后细胞表达5-HT2受体的mRNA,而不表达DRD2的mRNA.结论 DMSO/BHA可诱导hMSCs表达5-HT2受体基因,但不表达DRD2受体基因.  相似文献   

7.
目的研究缝隙连接在癫癎发病机制中的作用.方法以体外培养大鼠海马神经元为研究对象,采用免疫细胞化学方法和实时定量逆转录-聚合酶链反应(RT-PCR)方法观察缝隙连接蛋白(connexin, Cx)32和Cx43的表达,并加用生胃酮干预.结果神经元经无镁液处理1 h后Cx32 mRNA迅速升高,至5 h升高了近10倍;蛋白表达在2 h后开始增多(21.80±1.74),8 h后(47.30±5.75)较对照组(9.30±1.25)增高了5倍.Cx43水平低于Cx32,无镁液作用5 h后mRNA表达显著增多,8 h后蛋白表达始明显增强.生胃酮显著抑制了其表达.结论 Cx32和Cx43在癫癎样放电后表达显著增多,生胃酮能够抑制其表达和神经元放电,提示缝隙连接在癫癎的发生发展过程中具有重要的作用.  相似文献   

8.
目的 研究吗啡依赖形成及戒断对大鼠强啡肽原mRNA表达的影响。方法 将 18只Sprague Dawley雄性大鼠随机分为吗啡依赖组、吗啡戒断组和空白对照组 ,每组 6只。采用皮下注射吗啡建立大鼠吗啡依赖模型 ,初剂量为 10mg/kg ,以后每天增加 5mg/kg ,3次 /d ,连续 6天。应用放射性3 2 磷标记的三磷酸脱氧胞苷掺入标记探针法进行Northern印迹杂交技术检测三组大鼠强啡肽原mRNA的表达水平。结果  (1)连续 6天给予吗啡 ,吗啡依赖组大鼠下丘脑 (2 3 88± 1 6 2 )、纹状体(19 87± 2 0 3)及脊髓 (13 36± 1 4 6 )的强啡肽原mRNA相对含量分别低于对照组 (分别为 34 36±1 4 6、31 2 4± 2 83和 2 7 6 0± 2 89;均P <0 0 1) ,海马 (2 9 6 7± 3 2 3)强啡肽原mRNA相对含量高于对照组 (2 5 87± 1 74 ,P <0 0 5 ) ;(2 )给予纳洛酮处理 6 0min后 ,下丘脑 (10 2 2± 1 2 2 )、纹状体(5 90± 0 84 )、脊髓 (2 99± 0 4 8)强啡肽原mRNA的相对含量低于吗啡依赖组 (均P <0 0 1) ,而垂体强啡肽原mRNA(2 6 72± 1 79)却高于吗啡依赖组 (11 6 0± 2 2 4 ,P <0 0 1)。结论 慢性给予吗啡可影响大鼠强啡肽原mRNA的表达 ,从而参与吗啡依赖形成和戒断反应。  相似文献   

9.
背景:研究表明,激活素A作为神经细胞生存因子,参与神经损伤的保护作用以及维持海马神经元的存活。目的:观察激活素A对大脑皮层神经元长期存活及其对神经元电压依赖性钠电流的影响。设计、时间及地点:随机的细胞和分子生物学及电生理学实验,于2007-2009年在吉林大学白求恩医学院免疫学系完成。材料:孕17天小鼠购于吉林大学动物中心;小鼠源性Neuro-2a 细胞来自美国ATCC;人重组激活素A购于R&D公司。方法:①取孕17天小鼠胚胎的大脑皮层神经元进行原代培养,于加入5ng/ml 激活素A和4ng/ml NGF后的第1、3、5、7和9天进邢盍觳猓虎诩?ng/ml 激活素A对Neuro-2a 细胞Na+电流(INa)的影响;③RT-PCR检测激活素A对Neuro-2a细胞ActRII、VIP及iNOS mRNA表达的影响。主要观察指标:①台酚蓝染色观察活细胞,通过甲苯胺蓝染色尼氏小体计数神经元;②膜片钳实验记录全细胞INa。结果:①对照组存活的神经元呈现时间依赖性减少,在培养第7天,几乎没有存活的神经元,而NGF组和激活素A组在培养第9天仍有部分存活的神经元;②与对照组 INa (0.817±0.21 nA)相比较,激活素A增加Neuro-2a细胞INa (1.044±0.22 nA) (p< 0.05) (n=10);③激活素A诱导Neuro-2a细胞ActRIIA、ActRIIB 和VIP mRNA的表达,降低iNOS mRNA表达。结论:激活素A维持小鼠大脑皮层神经元长期存活,增加神经元电压依赖性Na+电流。  相似文献   

10.
目的研究中药单体成分红景天甙(salidroside)对1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)诱发的帕金森病(Parkinson disease,PD)小鼠模型的脑保护作用及其可能机制。方法80只C57BL雄性小鼠,分为正常对照组、MPTP模型组、MPTP+红景天甙组(即干预组,分别用3 mg/kg、50 mg/kg和150 mg/kg)及红景天甙对照组(分别用3 mg/kg、50 mg/kg和150 mg/kg),每组10只。应用免疫组化法观察黑质酪氨酸羟化酶(TH)阳性神经元数目变化,蛋白印迹法(Western blot)检测TH、胶质细胞源性神经营养因子(GDNF)、胶质纤维酸性蛋白(GFAP)在纹状体中表达水平的变化。结果在小鼠黑质部位,MPTP组TH阳性神经元数目明显少于正常对照组及干预组(P<0.05)。Western blot结果显示,不同剂量干预组小鼠纹状体中的TH蛋白表达(相对灰度值)(0.8326±0.0930.0.9007±0.0104和1.1114±0.2013)较MPTP组的TH蛋白表达(0.5738±0.01真4)明显增加(P< 0.05);干预组的GDNF蛋白表达(1.3503±0.0573)较MPFP组的蛋白表达(0.1485±0.0118)显著增加(P<0.05);干预组的GFAP蛋白表达(2.4788±0.2093)与MPTP组(1.8431±0.1559)之间差异无统计学意义(P>0.05),但是干预组较正常对照组(1.3695±0.1174)明显增加(P<0.05)。结论红景天甙可以拮抗MPTP诱导的PD模型小鼠黑质多巴胺能神经元的丢失,其神经保护作用可能与促进内源性GDNF分泌增加有关。  相似文献   

11.
Dahl  N. A.  Looney  G. A.  Black  W. H. 《Acta neuropathologica》1982,57(2-3):111-120
Summary This paper examines the neuropathology of oxygen-glucose deprivation uncomplicated by stagnant conditions. Rabbit vagus nerves were pulled into asmulti-compartment perfusion chamber, stimulated five times per second and deprived of energy by substituting nitrogen and deoxyglucose for oxygen and glucose in the Locke's perfusate. After incubation the compartments were perfused with gluteraldehyde solution, and the nerves were prepared for electron microscopy. Fixation in the compartments ensured precise cross and longitudinal sections which permitted quantitative comparisons. Although the action potentials ceased in 45 min, 1 h of energy deprivation did not significantly affect the ultrastructure. After 2 h of deprivation the axons were smaller and flattened and microtubules appeared packed together. In the smallest axons the microtubules were gone, the neurofilaments were compacted and the few mitochondria had a dense, homogenous appearance. By 4 h the shrinking was extreme, yet 8% were swollen much larger than any of the controls. Longitudinal views showed these balloned areas were greatly expanded regions of the smallest axons. Both tiny and huge regions were devoid of microtubules and the swollen axons contained expanded mitochondria.Calcium is indirectly implicated in the pathogenesis by the concurrence of mitochondrial alteration as the microtubules disappear coupled with the known role of mitochondria in calcium regulation and the reported effect of high calcium on microtubual dissociation. In is suggested that axons first shrink as osmotially active molecules are used or washed out. After a time without energy the mitochondria can no longer regulate the intracellular calcium, microtubules dissociate, and calcium-activated phospholipases create osmotically active molecules. Finally, high-amplitude, disruptive swelling occurs.Supported, in part, by a Grant-in-aid from the American Heart Association with funds contributed by the American Heart Association, Kansas Affiliate and by the University of Kansas Biomedical Sciences Support Grant RR0737  相似文献   

12.
目的探讨星形胶质细胞(astrocyte,AS)对天冬氨酸特异性半胱氨酸蛋白酶(cysteinyl aspartate specific proteinase,caspase)介导β淀粉样蛋白(β-amyloid,Aβ)早期突触毒性作用的影响,以期为进一步研究与血管性痴呆(vascular dementia,Va D)的发病机制奠定基础。方法以原代培养大鼠海马纯神经元体系(NE-S)及混合培养体系(MIX-S,主要包含神经元及AS)为研究对象,各体系分为6组:对照组、caspase-8抑制剂组、caspase-9抑制剂组、Aβ处理组、caspase-8抑制剂预处理加Aβ组和caspase-9抑制剂预处理加Aβ组。免疫荧光检测各组近胞体10μm段树突中突触后密度蛋白(postsynaptic density-95,PSD95)表达量的变化。结果 1在NE-S与MIX-S中,与对照组相比,caspase-8抑制剂组、caspase-9抑制剂组PSD95的表达量均无明显差异,Aβ处理组PSD95的表达量均显著降低(P均0.001)。2在NE-S中,与Aβ处理组相比,caspase-9抑制剂预处理加Aβ组PSD95的表达量显著回升至对照组水平,caspase-8抑制剂预处理加Aβ组则无显著改变;在MIX-S中的结果则相反,即caspase-8抑制剂预处理加Aβ组PSD95的表达量显著回升至对照组水平,而caspase-9抑制剂预处理加Aβ组则无显著改变。3MIX-S与NE-S两种培养系统间相比较,对照组间及Aβ处理组间PSD95的表达量均无显著差异,而caspase-8抑制剂预处理加Aβ组间及caspase-9抑制剂预处理加Aβ组间PSD95的表达量差异有显著性。结论在Aβ早期突触毒性作用中,AS参与caspase-8介导的死亡受体通路激活过程,且参与抑制神经元的线粒体通路。  相似文献   

13.
Genistein is one of several isoflavones that has a structure similar to 17β-estradiol, has a strong antioxidant effect, and a high affinity to estrogen receptors. At 15 weeks after ovariectomy, the expression of Bcl-2 in the hippocampus of rats decreased and Bax expression increased, with an obvious upregulation of apoptosis. However, intraperitoneal injection of genistein or 17β-estradiol for 15 consecutive weeks from the second day after operation upregulated Bcl-2 protein expression downregulated Bax protein expression, and attenuated hippocampal neuron apoptosis. Our experimental findings indicate that long-term intervention with genistein can lead to a decrease in apoptosis in hippocampal neurons following ovariectomy, upregulate the expression of Bcl-2, and downregulate the expression of Bax. In addition, genistein and 17β-estradiol play equal anti-apoptotic and neuroprotective roles.  相似文献   

14.
Voxel-based morphometry can be used to quantitatively compare structural differences and functional changes of gray matter in subjects.In the present study,we compared gray matter images of 32 patients with Parkinson’s disease and 25 healthy controls using voxel-based morphometry based on 3.0 T high-field magnetic resonance T1-weighted imaging and clinical neurological scale scores.Results showed that the scores in Mini-Mental State Examination and Montreal Cognitive Assessment were lower in patients compared with controls.In particular,the scores of visuospatial/executive function items in Montreal Cognitive Assessment were significantly reduced,but mean scores of non-motor symptoms significantly increased,in patients with Parkinson’s disease.In addition,gray matter volume was significantly diminished in Parkinson’s disease patients compared with normal controls,including bilateral temporal lobe,bilateral occipital lobe,bilateral parietal lobe,bilateral frontal lobe,bilateral insular lobe,bilateral parahippocampal gyrus,bilateral amygdale,right uncus,and right posterior lobe of the cerebellum.These findings indicate that voxel-based morphometry can accurately and quantitatively assess the loss of gray matter volume in patients with Parkinson’s disease,and provide essential neuroimaging evidence for multisystem pathological mechanisms involved in Parkinson’s disease.  相似文献   

15.
Positron emission tomography (PET) is an in vivo molecular imaging tool which is widely used in nuclear medicine for early diagnosis and treatment follow-up of many brain diseases. PET uses biomolecules as probes which are labeled with radionuclides of short half-lives, synthesized prior to the imaging studies. These probes are called radiotracers. Fluorine-18 is a radionuclide routinely used in the radiolabeling of neuroreceptor ligands for PET because of its favorable half-life of 109.8 min. The delivery of such radiotracers into the brain provides images of transport, metabolic, and neurotransmission processes on the molecular level. After a short introduction into the principles of PET, this review mainly focuses on the strategy of radiotracer development bridging from basic science to biomedical application. Successful radiotracer design as described here provides molecular probes which not only are useful for imaging of human brain diseases, but also allow molecular neuroreceptor imaging studies in various small-animal models of disease, including genetically-engineered animals. Furthermore, they provide a powerful tool for in vivo pharmacology during the process of pre-clinical drug development to identify new drug targets, to investigate pathophysiology, to discover potential drug candidates, and to evaluate the pharmacokinetics and pharmacodynamics of drugs in vivo.  相似文献   

16.
Understanding the pathway for amyloid percursor protein (APP) catabolism has become an important line of investigation. APP is a ubiquitous membrane bound protein that is rapidly cleaved at the membrane, yielding a secreted protein identical to protease nexin II and an internalized 11.5 kDa 100 residue C terminal derivative (CTD). The levels of CTDs in a variety of cell lines have been examined and were found to differ. Cell types associated with the pathology of Alzheimer's disease (AD), such as olfactory neuroblasts (ON) and cortical vascular endothelial cells, have higher levels of CTDs than lymphoblasts and melanoma cells. The mechanism of CTD catabolism appears to involve the lysosome because blockade of lysosomal but not endosomal or mitochondrial function results in increased levels of CTDs. Under these conditions, production of larger, amyloidogenic CTDs is also seen. In cells possessing higher levels of CTDs we find that the mechanism for production of amyloidogenic CTDs may involve the internalization of intact full-length APP. Thus, inhibition of the lysosomal system appears capable of generating amyloidogenic peptides. The amount of amyloidogenic peptides appears to vary among cell lines. Such variation may shed light on why amyloid accumulates around specific cell types such as vascular endothelial cells, neurons, and glia. Finally, disfunction of the lysosomal system may play a role in the pathogenesis of Alzheimer's disease.  相似文献   

17.
IntroductionWe report further validation and normative data for the THINC‐Integrated Tool (THINC‐it), a measure of cognitive function designed for use with individuals living with Major Depressive Disorder, but which is finding use in further psychiatric and neurological diseases. THINC‐it comprises four objective computerised cognitive tests based on traditional psychological paradigms and a version of the Perceived Deficits Questionnaire assessment.MethodsSample size of n = 10.019 typical control study participants were tested on one to two occasions to further validate the reliability of THINC‐it. Temporal reliability was assessed across 120–180 days.ResultsTest‐retest reliability correlations varied between r = 0.50 and 0.72 for the component measures and r = 0.75 (95% confidence intervals 0.74, 0.76) for the THINC‐it composite score. Normative data categorised by Age, Sex and Years of Education were calculated and the effect on task performance was reported.DiscussionOur analysis confirms previously reported levels of reliability and validates previously reported normative data values.  相似文献   

18.
Most hypotheses concerning the mechanisms underlying Parkinson’s disease are based on altered synaptic transmission of the nigrostriatal system.However,extrasynaptic transmission was recently found to affect dopamine neurotransmitter delivery by anisotropic diffusion in the extracellular matrix,which is modulated by various extracellular matrix components such as fibronectin.The present study reviewed the neuroprotective effect of fibronectin in extrasynaptic transmission.Fibronectin can regulate neuroactive substance diffusion and receptor activation,and exert antineuroinflammatory,adhesive and neuroprotective roles.Fibronectin can bind to integrin and growth factor receptors to transactivate intracellular signaling events such as the phosphatidylinositol 3-kinase/protein kinase B pathway to regulate or amplify growth factor-like neuroprotective actions.Fibronectin is assembled into a fibrillar network around cells to facilitate cell migration,molecule and ion diffusion,and even drug delivery and treatment.In addition,the present study analyzed the neuroprotective mechanism of fibronectin in the pathogenesis of Parkinson’s disease,involving integrin and growth factor receptor interactions,and discussed the possible therapeutic and diagnostic significance of fibronectin in Parkinson’s disease.  相似文献   

19.
Neuroacanthocytosis is an autosomal recessive or dominant inherited disease characterized by widespread, non-specific nervous system symptoms, or spiculated "acanthocytic" red blood cells. The clinical manifestations typically involve chorea and dystonia, or a range of other movement disorders. Psychiatric and cognitive symptoms may also be present. The two core neuroacanthocytosis syndromes, in which acanthocytosis is atypical, are autosomal recessive chorea-acanthocytosis and X-linked McLeod syndrome. Acanthocytes are found in a smaller proportion of patients with Huntington’s disease-like 2 and pantothenate kinase-associated neurodegeneration. Because the clinical manifestations are diverse and complicated, in this review we present features of inheritance, age of onset, neuroimaging and laboratory findings, as well as the spectrum of central and peripheral neurological abnormalities and extraneuronal involvement to help distinguish the four specific syndromes.  相似文献   

20.
王聪杰  李虹  郑丽  刘珊  卢海丽  陈娜  张斌  周衡 《中国卒中杂志》2021,16(10):1044-1049
目的 观察rt-PA静脉溶栓联合双重抗血小板治疗轻型缺血性卒中的有效性及安全性。 方法 以2013年12月-2016年12月在石家庄市第一医院连续住院治疗的轻型缺血性卒中患者为研究 对象,将其随机分为对照组、溶栓+单抗组和溶栓+双抗组。对照组不进行静脉溶栓,长期口服阿 司匹林(100 mg/d)抗血小板治疗;溶栓+单抗组在rt-PA静脉溶栓(0.9 mg/kg,最大剂量90 mg)基 础上长期单用阿司匹林(100 mg/d)抗血小板治疗;溶栓+双抗组在溶栓后单抗基础上加用氯吡格雷 (75 mg/d)双重抗血小板治疗,双抗治疗21 d后改为阿司匹林长期单抗治疗。随访3个月,有效性指标 为3个月时NIHSS 0~1分、Barthel指数(Barthel index,BI)95~100分和mRS 0~1分的比例,3个月时缺 血性卒中的复发率;安全性指标为治疗24 h出血转化和症状性出血转化的发生率。另外比较三组间 基线和3个月时血清hs-CRP和IL-6的水平差异。 结果 研究共纳入85例患者,对照组28例,溶栓+单抗组28例,溶栓+双抗组29例,全部患者均完 成3个月随访,无死亡患者。对照组、溶栓+单抗组和溶栓+双抗组3个月随访时NIHSS 0~1分比例分 别为46.43%、78.57%和93.10%,BI 95~100分比例分别为53.57%、82.14%和89.66%,mRS 0~1分 的比例分别为50.00%、82.14%和93.10%,三组上述有效性指标差异均有统计学意义,两两比较显 示,溶栓+双抗组高于溶栓+单抗组和对照组,溶栓+单抗组高于对照组,差异均有统计学意义;对 照组、溶栓+单抗组和溶栓+双抗组3个月时缺血性卒中复发率分别为32.14%、7.14%和3.45%,差异 有统计学意义。安全性指标方面,三组均无出血转化事件。对照组、溶栓+单抗组和溶栓+双抗组3 个月时的hs-CRP水平分别为11.92±3.58 mg/L、9.04±2.85 mg/L和6.04±2.65 mg/L,IL-6水平分别为 26.18±4.65 ng/L、16.11±6.93 ng/L和12.84±2.57 ng/L,三组上述炎症因子水平差异均有统计学意 义,其中溶栓+双抗组低于溶栓+单抗组和对照组,溶栓+单抗组低于对照组。 结论 对于急性轻型缺血性卒中患者,rt-PA静脉溶栓治疗后短期双重抗血小板治疗可显著改善患 者神经功能,降低炎症因子水平,降低复发率,且不增加出血风险。  相似文献   

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