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1.
《中风与神经疾病杂志》2015,(8):688-690
目的探讨槲皮苷对H2O2所致的PC12细胞凋亡的保护作用及机制。方法 PC12细胞培养后,MTT检测细胞存活率的方法进行H2O2损伤模型的摸索和槲皮苷药物浓度的筛选,将PC12细胞分为对照组、模型组和不同剂量槲皮苷组。用400μmol H2O2刺激PC12神经元细胞使其发生凋亡复制阿尔茨海默病(AD)模型,MTT法检测PC12细胞存活率、硫辛酰胺脱氢酶催化的INT显色反应检测乳酸脱氢酶(LDH)释放量和DAPI荧光核染色观察细胞凋亡形态学改变,Western blot方法检测Cytc和caspase-3表达的变化。结果 400μmol H2O2诱导PC12细胞损伤明显,与模型组比较,槲皮苷组PC12细胞存活率显著提高(P<0.01),凋亡率显著下降(P<0.01),LDH释放量和凋亡相关蛋白Cytc和caspase-3的表达显著减少(P<0.01)。结论槲皮苷可抑制H2O2诱导的PC12细胞凋亡,其机制可能与抑制细胞凋亡线粒体途径中凋亡相关蛋白Cytc和caspase-3的表达有关。 相似文献
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目的探讨芍药苷(PF)对6羟基多巴胺(6-OHDA)损害的PC12细胞的保护作用。方法检测各组6-OHDA诱导PC12损伤细胞相对存活率和乳酸脱氢酶(LDH)活性;采用免疫荧光和免疫印迹技术检测PC12细胞α-突触核蛋白(α-syn)、自噬相关蛋白(LC3-Ⅱ、p62)以及酸敏感离子通道(ASIC1a)的蛋白水平。结果与正常对照组比较,6-OHDA组相对细胞存活率显著下降,LDH活性显著升高(均P0.01)。与6-OHDA组比较,Pc Tx1组、阿米洛利组、PF各亚组相对细胞存活率均显著升高,LDH活性显著降低(P0.05~0.01)。与正常对照组比较,6-OHDA组ASIC1a蛋白水平显著升高(P0.01)。与6-OHDA组比较,Pc Tx1组、阿米洛利组、PF各亚组ASIC1a蛋白水平均显著降低(P0.05~0.01)。与正常对照组比较,6-OHDA组α-syn、LC3-Ⅱ、p62蛋白水平均显著增加(均P0.01)。与6-OHDA组比较,Pc Tx1组、阿米洛利组、PF各亚组α-syn、LC3-Ⅱ、p62蛋白水平均显著降低(P0.05~0.01)。结论 PF可能通过提高α-syn的自噬性降解,对6-OHDA毒素损害的PC12细胞起到保护作用。PF的神经保护作用可能与抑制ASIC1a的活性有关。 相似文献
3.
目的探讨经过氧化氢(H_2O_2)损伤干预下Rab30在PC12细胞中的表达及可能的促凋亡通路。方法将体外常规培养的PC12细胞分为正常组和H_2O_2组。采用MTT检测细胞存活率;Annexin V-FITC/PI双染法检测细胞凋亡率;Western-blot检测Rab30、JNK3、GM130、Caspase-3的蛋白表达情况。结果 H_2O_2损伤干预可导致PC12细胞的存活率显著降低(P0.05),早期凋亡率和总凋亡率均显著增高(均P0.05);JNK3、Caspase-3蛋白表达水平在PC12细胞中显著增加(P0.05),而Rab30、GM130蛋白表达显著下降(P0.05)。结论 H_2O_2在PC12细胞中的促凋亡通路可能是H_2O_2激活JNK3的表达而靶向下调Rab30,致使高尔基体结构破碎,并激活Caspase-3的活性,从而诱导PC12细胞的凋亡。 相似文献
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目的 探讨莱菔硫烷对体外1-甲基-4-苯基吡啶离子(MPP+)诱导的PC12细胞氧化损伤模型是否具有保护作用及其机制.方法 以MPP+损伤PC12细胞制备氧化损伤模型.不同浓度的莱菔硫烷加入培养基观察各组细胞生长情况.后续实验分成4组:正常对照组(A)、莱菔硫烷组(B)、MPP+损伤组(C)、莱菔硫烷预处理+MPP+损伤组(D).通过MTT比色法检测细胞活力,观察不同浓度莱菔硫烷预处理PC12细胞活力变化及不同分组PC12细胞活力变化;流式细胞术检测不同分组PC12细胞中细胞凋亡率的变化;免疫印迹法测定不同分组PC12细胞内转录因子相关因子2(Nrf2)、血红素加氧酶1(HO-1)及醌还原氧化酶1(NQ01)蛋白的表达变化.结果 A组细胞存活率(98.70%)与MPP+(500μmol/L)组(58.16%)相比差异有统计学意义(F =21.83,P<0.05),D组细胞存活率明显提高.C组细胞凋亡率升高,D组细胞与C组相比差异有统计学意义,莱菔硫烷预处理后细胞凋亡率明显减低.C组Nrf2、HO-1、NQ01蛋白表达下降,D组Nrf2、HO-1、NQ01蛋白表达升高.结论 莱菔硫烷对MPP+诱导的PC12细胞损伤具有保护作用,莱菔硫烷对MPP+诱导的PC12细胞损伤的保护作用可能通过激活Nrf2-抗氧化反应元件通路途径实现. 相似文献
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目的探讨利福平对1-甲基-苯基-吡啶离子(MPP+)诱导的大鼠嗜铬细胞瘤细胞株(PC12)细胞形态、线粒体结构的影响。方法利用MPP+诱导分化PC12细胞建立帕金森病体外细胞模型;Hoechst33342荧光染色法检测细胞凋亡;透射电子显微镜观察各组细胞线粒体超微结构。结果正常细胞组PC12细胞形态完整,线粒体结构完整清晰;MPP+作用后,凋亡细胞数量增多,核固缩、碎裂明显,线粒体空泡化明显,部分细胞见凋亡小体形成;利福平作用后,随着利福平浓度的增高,细胞凋亡程度及线粒体空泡化现象明显减轻,且存在浓度依赖性。结论利福平可减轻MPP+所致PC12细胞线粒体损伤的程度,推测可能是通过对线粒体的保护作用来减轻MPP+诱导的分化PC12细胞的凋亡,但其作用的具体途径还需进一步研究。 相似文献
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目的探讨促红细胞生成素(erythropoietin,EPO)对1-甲基-4-苯基吡啶离子(MPP+)诱导的PC12细胞变性损伤的保护作用及机制。方法用MPP+处理PC12细胞制作帕金森病细胞模型,采用四甲基偶氮唑蓝法检测暴露于不同浓度EPO后细胞的活性;流式细胞术与DNA断端原位标记法(terminal deoxynucleotidyl transferase dUTPnick end labeling, TUNEL)检测各组的细胞凋亡率;免疫印迹法检测不同处理组PC12细胞Bcl-2和Bax的表达,并采用荧光法观察不同处理组PC12细胞活性氧(reactive oxygen species,ROS)与线粒体膜电位水平以及caspase-3活性的变化。结果 MPP+可以使PC12细胞存活率下降,凋亡率增高;同时PC12细胞内ROS增多,线粒体膜电位下降。MPP+还可以明显地提高Bax/Bcl-2比值并激活caspase-3。而EPO可以抑制这些由MPP+引发的改变,并在1 U/mL时发挥最大保护作用。结论 EPO可抑制MPP+诱导的PC12细胞死亡,其作用机制可能与其自身抗氧化和抗凋亡的特性有关。 相似文献
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14-3-3蛋白过表达减轻1-甲基-4-苯基吡啶离子对PC12细胞的毒性(英文) 总被引:1,自引:0,他引:1
目的研究14-3-3蛋白过表达对1-甲基-4苯基吡啶离子(MPP )诱导的PC12细胞死亡的影响作用及其可能的机制。方法构建pcDNA3.1( )-14-3-3 真核表达质粒,用脂质体2000转染PC12细胞;Western blot技术检测PC12细胞中14-3-3蛋白、Bcl-2 蛋白, 和BAD蛋白的表达;然后分别用MTT法、酶标仪及流式细胞仪检测PC12细胞的活力、caspase的活性及PC12细胞的凋亡率。结果(1)将pcDNA3.1( )-14-3-3质粒转染PC12细胞3周后,14-3-3蛋白的表达显著增加;(2)MPP 诱导PC12细胞存活率的下降是剂量依赖性的,当MPP 的浓度达100 μmol/L时,PC12细胞的存活率丧失约50%;(3)caspase 的活性随着MPP 浓度的增加而增高,当MPP 浓度到达100 μmol/L时caspase的活性也到达最大值,而当MPP 浓度超过100 μmol/L时,caspase的活性急剧下降;(4)用100 μmol/L 的MPP 处理PC12细胞24 h后,PC12细胞的凋亡率为26.5%,14-3-3蛋白的过表达使PC12细胞的凋亡率下降到8.6%;(5)用100 μmol/L MPP 处理PC12细胞后,Bcl-2蛋白的表达趋于下调而BAD蛋白的表达上调,14-3-3蛋白的过表达能显著的增加Bcl-2蛋白的表达而使BAD蛋白的表达下调。结论14-3-3蛋白过表达通过上调Bcl-2蛋白的表达并下调BAD蛋白的表达,减少了MPP 诱导的PC12细胞的凋亡,从而发挥对PC12细胞的保护作用。这些结果可能为PD的治疗提供新的药物靶点。 相似文献
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目的观察蛇床子素(osthole)对1-甲基-4-苯基吡啶离子(MPP+)诱导PC12细胞损伤的神经保护作用。方法将MPP+加入培养的PC12细胞中,建立多巴胺能神经元损伤模型,加入不同浓度的蛇床子素预处理细胞(0.01、0.05、0.1mmol/L)。处理24h后用噻唑蓝(MTT)比色法检测细胞活性;以乳酸脱氢酶(LDH)活性测定反映细胞的损伤程度;采用Westernblot法检测Bax、Bcl-2蛋白的表达,分析Bax/Bcl-2比值变化,以及检测细胞色素C的改变。结果蛇床子素可以明显减少MPP+诱导的PC12细胞活性的降低,LDH的释放,Bax/Bcl-2比值的增高以及细胞色素C的释放(P〈0.05)。结论蛇床子素对MPP+诱导的PC12细胞损伤具有保护作用。 相似文献
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目的 探讨乌司他丁对缺氧诱导PC12细胞神经损伤的作用及分子机制。方法 PC12细胞分为对照组、缺氧组、缺氧+乌司他丁低、中、高剂量组、缺氧+miR-NC组、缺氧+miR-190组、缺氧+乌司他丁+anti-miR-NC组、缺氧+乌司他丁+anti-miR-190组。检测培养液中乳酸脱氢酶(LDH)漏出率及细胞中超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量;流式细胞术检测细胞凋亡;蛋白质印迹法(Western blotting)检测蛋白表达;实时荧光定量聚合酶链反应(qRT-PCR)检测miR-190表达水平。结果 与缺氧组比较,缺氧+乌司他丁低、中、高剂量组PC12细胞中LDH漏出率降低,SOD活性升高,MDA含量降低,细胞凋亡率降低,Bcl-2相对表达量升高,Bax相对表达量降低,miR-190相对表达量升高,且呈剂量依赖性(均P<0.05)。miR-190过表达后,LDH漏出率降低,SOD活性升高,MDA含量降低,细胞凋亡率降低,Bcl-2相对表达量升高,Bax相对表达量降低(均P<0.05)。抑制miR-190表达能逆转乌司他丁对缺氧诱导的PC12细胞损伤的作用。结论 乌司他丁可能通过上调miR-190表达对缺氧诱导PC12细胞神经损伤起保护作用。 相似文献
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目的 研究落新妇苷对H2O2诱导的氧化应激损伤的PC12细胞影响。方法 将PC12细胞分为5组:对照组、H_2O_2组及不同浓度(1μmol/L、10μmol/L、20μmol/L)落新妇苷组。采用CCK8实验检测各组细胞的活力; Annexin V-FITC/PI细胞凋亡实验检测各组细胞凋亡率; Western blot检测PI3K、AKT、Caspase3和P38蛋白及其磷酸化激活蛋白的表达水平。结果 与H_2O_2组相比,落新妇苷组细胞的活力显著提高,细胞凋亡率明显降低,活化的凋亡相关蛋白Cleaved Caspase3表达水平降低,PI3K/AKT途径相关蛋白p-PI3K和p-AKT的表达水平升高,P38 MAPK途径重要蛋白p-P38的表达水平降低。结论 落新妇苷对H_2O_2诱导的氧化应激损伤的PC12细胞有明显保护作用;这种保护作用可能是通过激活PI3K/AKT信号通路及抑制P38MAPK信号通路实现的。 相似文献
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目的观察长春西汀联合氟西汀治疗脑卒中后抑郁症的临床疗效,初步探讨其作用机制。方法选择临床确诊为脑卒中后抑郁症患者120例,采用随机对照方法,分为长春西汀联合氟西汀治疗组(观察组)与氟西汀治疗组(对照组),每组60例,疗程4周。治疗前及治疗2、4周后通过神经功能缺损评分(NIHSS)以及汉密尔顿抑郁量表(HAMD)评定疗效。采用荧光分光光度计法测定血清单胺类递质的水平。结果治疗2、4周末,观察组和对照组经HAMD及NIHSs评分比较,治疗前两组评分均下降(P〈0.05);且观察组低于对照组(P〈0.05)。观察组总体疗效优于对照组(P〈0.05)。治疗前两组血清NE、DA、5-HT含量差异无统计学意义;治疗2、4周末,与治疗前相比,两组血清NE、DA、5-HT含量均有升高(P〈0.05),且观察组高于对照组(P〈0.05)。在用药安全性上,两组中治疗前后均未出现明显不良事件。结论长春西汀联合氟西汀治疗脑卒中后抑郁症能显著提高脑卒中后抑郁症患者的疗效,且无明显不良反应。作用机制可能与提高血清单胺类神经递质水平有关。 相似文献
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目的观察阿伐他汀(Atorvastatin)对EAE的治疗作用并初探其治疗机制。方法以豚鼠脑、脊髓为原料提取髓鞘碱性蛋白MBP,免疫Lewis大鼠建立EAE模型。建模后每日对大鼠神经症状进行评分,采用ELISA法检测大鼠脾细胞培养上清液中IFN-γ、IL-12和IL-4水平。结果与EAE组相比,Atorvastatin组大鼠发病时间有所延迟,症状有不同程度减轻。与正常组相比,EAE组大鼠17d、21d时,IL-4水平明显升高(P〈0.01),13,17,21d时IFN-γ、IL-12水平均明显升高(P〈0.01);IFN-γ、IL-12浓度与神经症状评分有较强的正相关关系(RIFN-γ=0.904,P〈0.01;RIL-12=0.885,P〈0.01)。与EAE组相比,Atorvastatin组13d、17d时IL-4水平明显升高(P〈0.01)。IFN-γ、IL-12水平在13,17,21d时均显著低于EAE组(P〈0.05)。结论Alorvastalin能改善EAE大鼠的症状,其机制可能与纠正Th1/Th2失衡有关。 相似文献
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何跃 《神经疾病与精神卫生》2011,11(3):300-303
转化障碍是指随意运动和特殊感觉方面的功能障碍,但是不能用器质性疾病所解释,转化障碍可以单独存在,也可与其他器质性神经疾病共存.对大多数临床医生来说,转化障碍是一个既模糊又陌生的概念,因此临床误诊率较高,若持续存在预后较差.为了增进对这种复杂障碍的认识和处理,本文从临床及防治方面作一综述. 相似文献
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垂体腺瘤发病机制仍不明确.本文从癌基因、抑癌基因、下丘脑神经激素细胞信号通路、生长因子细胞信号通路、外周激素反馈细胞信号通路等方面对垂体腺瘤发病机制相关研究进展进行综述. 相似文献
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Yinghong Li Zhengzhi Wu Andrew C. J. Huang Ming Li XiaoLi Zhang Jiguo Wang 《中国神经再生研究》2009,4(2):85-91
BACKGROUND: Neuronal loss, synapse mutilation, and increasing malnourished axons are pathologically related to Alzheimer's disease. Microtubule-associated protein 2 (MAP2) is of importance for neuronal, axonal, and dendritic generation, extension, and stabilization, as well as for the regulation of synaptic plasticity.
OBJECTIVE: To investigate the antagonistic effects of natural-cerebrolysin-containing serum on beta amyloid protein 1-40 (Aβ1-40)-induced neurotoxicity from the standpoints of cell proliferation, synaptogenesis, and cytoskeleton formation (MAP2 expression). DESIGN, TIME AND SETTING: A paralleled, controlled, neural cell, and molecular biology experiment was performed at the Institute of Integrated Chinese and Western Medicine, Shenzhen Hospital, Southern Medical University between February 2006 and April 2008.
MATERIALS: PC12 cells, derived from the rat central nervous system, were purchased from Shanghai Institute of Cell Biology, Chinese Academy of Sciences, China. A β1-40 was provided by Sigma, USA. Natural-cerebrolysin was provided by Shenzhen Institute of Integrated Chinese and Western Medicine, China. The natural-cerebrolysin was predominantly composed of Renshen (Radix Ginseng), Tianma (Rhizoma Gastrodiae), and Yixingye (Ginkgo Leaf) in a proportion of 1:2:2. Following conventional water extraction technology, an extract (1:20) was prepared. Each gram of extract equaled 20 grams of crude drug. In a total of 12 adult male New Zealand rabbits, six underwent intragastric administration of natural-cerebrolysin extract for 1 month to prepare natural-cerebrolysin-containing serum, and the remaining six rabbits received intragastric administration of physiological saline to prepare normal blank serum.
METHODS: An AIzheimer's disease in vitro model was induced in PC12 cells using Aβ1-40. The cells were incubated with varying doses of natural-cerebrolysin-containing serum (2.5%, 5%, and 10%). Normal blank serum-treated PC12 cells served as a blank control group.
MAIN OUTCOME MEASURES: Through the use of inverted phase contrast microscope, cell morphology and neurite growth were observed, neurite length was measured, and the percentage of neurite-positive cells was calculated. Cell proliferation rate was determined by MTT assay, and MAP 2 expression was detected by fluorescent immunocytochemistry.
RESULTS: Following Aβ1-40 treatments, some PC12 cells were apoptotic/dying, and only a few short neurites were observed. Following interventions with natural-cerebrolysin-containing serum, the PC12 cells proliferated, there was an increased number of neurites, and neurite length was enhanced. After middle- and high-dose natural-cerebrolysin treatments, the percentage of neurite-positive cells, as well as the average length of neurites, was significantly greater than the normal blank serum-treated PC12 cells (P 〈 0.05 or P 〈 0.01). Compared with the blank control group, MAP2 expression in the Aβ1-40-treated PC12 cells was significantly inhibited, and the cell proliferation rate was significantly decreased (P 〈 0.01). Following incubations with natural-cerebrolysin-containing serum, MAP2 expression and cell proliferation rate in the PC12 cells were significantly increased in a dose-dependent manner, compared with treatments with blank control serum (P 〈 0.05 or P 〈 0.01 ).
CONCLUSION: Natural-cerebrolysin exhibited antagonistic effects on neurotoxicity in Aβ1-40 induced Alzheimer's disease in vitro models. These effects were likely related to cell proliferation and the upregulation of intracellular MAP2 expression. 相似文献
OBJECTIVE: To investigate the antagonistic effects of natural-cerebrolysin-containing serum on beta amyloid protein 1-40 (Aβ1-40)-induced neurotoxicity from the standpoints of cell proliferation, synaptogenesis, and cytoskeleton formation (MAP2 expression). DESIGN, TIME AND SETTING: A paralleled, controlled, neural cell, and molecular biology experiment was performed at the Institute of Integrated Chinese and Western Medicine, Shenzhen Hospital, Southern Medical University between February 2006 and April 2008.
MATERIALS: PC12 cells, derived from the rat central nervous system, were purchased from Shanghai Institute of Cell Biology, Chinese Academy of Sciences, China. A β1-40 was provided by Sigma, USA. Natural-cerebrolysin was provided by Shenzhen Institute of Integrated Chinese and Western Medicine, China. The natural-cerebrolysin was predominantly composed of Renshen (Radix Ginseng), Tianma (Rhizoma Gastrodiae), and Yixingye (Ginkgo Leaf) in a proportion of 1:2:2. Following conventional water extraction technology, an extract (1:20) was prepared. Each gram of extract equaled 20 grams of crude drug. In a total of 12 adult male New Zealand rabbits, six underwent intragastric administration of natural-cerebrolysin extract for 1 month to prepare natural-cerebrolysin-containing serum, and the remaining six rabbits received intragastric administration of physiological saline to prepare normal blank serum.
METHODS: An AIzheimer's disease in vitro model was induced in PC12 cells using Aβ1-40. The cells were incubated with varying doses of natural-cerebrolysin-containing serum (2.5%, 5%, and 10%). Normal blank serum-treated PC12 cells served as a blank control group.
MAIN OUTCOME MEASURES: Through the use of inverted phase contrast microscope, cell morphology and neurite growth were observed, neurite length was measured, and the percentage of neurite-positive cells was calculated. Cell proliferation rate was determined by MTT assay, and MAP 2 expression was detected by fluorescent immunocytochemistry.
RESULTS: Following Aβ1-40 treatments, some PC12 cells were apoptotic/dying, and only a few short neurites were observed. Following interventions with natural-cerebrolysin-containing serum, the PC12 cells proliferated, there was an increased number of neurites, and neurite length was enhanced. After middle- and high-dose natural-cerebrolysin treatments, the percentage of neurite-positive cells, as well as the average length of neurites, was significantly greater than the normal blank serum-treated PC12 cells (P 〈 0.05 or P 〈 0.01). Compared with the blank control group, MAP2 expression in the Aβ1-40-treated PC12 cells was significantly inhibited, and the cell proliferation rate was significantly decreased (P 〈 0.01). Following incubations with natural-cerebrolysin-containing serum, MAP2 expression and cell proliferation rate in the PC12 cells were significantly increased in a dose-dependent manner, compared with treatments with blank control serum (P 〈 0.05 or P 〈 0.01 ).
CONCLUSION: Natural-cerebrolysin exhibited antagonistic effects on neurotoxicity in Aβ1-40 induced Alzheimer's disease in vitro models. These effects were likely related to cell proliferation and the upregulation of intracellular MAP2 expression. 相似文献
16.
Mingshan Wang Lina Zhang Xiangyu Ji Yanwei Yin Hui Xu Hong Liu Nianguo Hou 《中国神经再生研究》2009,4(12):1013-1018
BACKGROUND: Previous studies of cerebral ischemia have used young animals, with an ischemic time greater than 5 minutes (safe time limit). Despite an increased understanding of neuronal apoptosis, it remains uncertain whether brief cerebral ischemic events of 5 minutes or less damage brain tissue in elderly rodents. OBJECTIVE: To investigate the effects of transient cerebral ischemia (5 minutes)/reperfusion injury on brain cortical and hippocampal edema, aquaporin-4 (AQP-4) expression, and neuronal apoptosis in aged rats, and to compare ischemic sensitivity between cortex and hippocampus. DESIGN, TIME AND SETTING: A randomized, controlled, animal experiment was performed at the Institute of Cerebrovascular Disease, Qingdao University Medical School from April 2008 to March 2009. MATERIALS: Rabbit anti-AQP-4 polyclonal antibody, TUNEL kit, and SABC immunohistochemistry kit were purchased from Wuhan Boster Bioengineering, China. METHODS: A total of 160 healthy, male, aged 19-21 months, Wistar rats were randomly assigned to 4 groups: sham-surgery, and ischemia 1-, 3-, and 5-minute groups, with 40 rats in each group. The global cerebral ischemia model was established using the Pusinelli four-vessel occlusion, and the three cerebral ischemia groups were subdivided into reperfusion 12-hour, 1-, 2-, 3-, and 7-day subgroups, with 8 rats in each subgroup. The sham-surgery group was subjected to exposure of the first cervical bilateral alar foramina and bilateral common carotid arteries. MAIN OUTCOME MEASURES: The dry-wet weight assay was used to measure brain water content and histopathology of the cortex and hippocampus was observed following hematoxylin-eosin staining. In addition, cortical and hippocampal AQP-4 expression was detected by streptavidin-biotin complex immunohistochemistry, and neuronal apoptosis was detected by the TUNEL method. RESULTS: There was no significant difference in brain water content or AQP-4 expression in the cortex and hippocampus between ischemia 1- and 3-minute groups and the sham-surgery group or brain water content or AQP-4 expression in the cortex between ischemia 5-minute group and sham-surgery group (P 〉 0.05). However, brain water content and AQP-4 expression in the hippocampus after 5 minutes of cerebral ischemia were significantly increased compared with the sham-surgery group (P 〈 0.05 or P 〈 0.01). Several TUNEL-positive cells were observed in the cortex and hippocampus of the sham-surgery group and ischemia 1-minute group, as well as in the cortex of the ischemia 3-minute group. In addition, the number of apoptotic neurons in the hippocampus of ischemia 3-minute group and in the cortex and hippocampus of ischemia 5-minute group was significantly increased (P 〈 0.05 or P 〈 0.01 ). Neuronal apoptosis was increased after 12 hours of ischemia/reperfusion, and it reached a peak by 2 days (P 〈 0.01). CONCLUSION: Transient cerebral ischemia (5 minutes) resulted in increased hippocampal edema, AQP-4 expression, and neuronal apoptosis. Moreover, cerebral ischemia had a greater effect on neuronal apoptosis than brain edema or AQP-4 expression, and the hippocampus was more sensitive than the cortex. 相似文献
17.
注意力缺陷伴多动障碍(ADHD)的确切病因还不十分清楚,已有证据表明是一种遗传异质性疾病,由遗传和环境因素共同作用造成,本文综述了ADHD的遗传家系研究及执行功能和基因研究的进展。 相似文献
18.
墨蝶呤还原酶(SPR)催化四氢生物蝶呤(BH4)从头合成途径的最后一步反应。SPR基因遗传缺陷或突变可导致BH。的合成紊乱,影响单胺类神经递质(如多巴胺、5-羟色胺及谷氨酸等)的合成或释放,进而参与包括精神分裂症在内的多种神经精神系统疾病的发生发展过程。此外,SPR基因敲除小鼠表现出持续增强的自主活动等类精神分裂症症状,说明该基因在精神分裂症的发病中扮演重要的角色。进一步研究SPR基因及其单核苷酸多态性的功能,可为阐明精神分裂症的发病机制提供重要的线索,也为新一代抗精神病药物的研制及开发开拓新的视野。现对SPR基因与精神分裂症的相关研究做一综述。 相似文献
19.
目的 探讨首发青少年抑郁症患者家庭环境、应付方式的特点及两者的关系.方法 采用家庭环境量表中文版(FES-CV)、应付方式问卷,对30例首发青少年抑郁症患者及30例正常对照者进行测评.结果 (1)青少年抑郁症患者家庭环境中亲密度、情感表达、知识性、娱乐性、宗教道德观等因子分低于正常对照组,矛盾性因子分高于正常对照组(P<0.05);(2)青少年抑郁症组应付方式中的解决问题、求助因子分低于正常对照组,自责、退避因子分高于正常对照组(P<0.05);(3)青少年抑郁症组应付方式中的解决问题因子与家庭环境中的控制性呈正相关(r=0.42);求助因子与情感表达呈正相关(r=0.41);自责因子与亲密度、情感表达呈负相关(r =-0.48,r =-0.44),与矛盾性呈正相关(r=0.47).结论 青少年抑郁症患者更多采用不成熟的应付方式,并与不良的家庭环境有关. 相似文献
20.