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排序方式: 共有125条查询结果,搜索用时 15 毫秒
1.
目的 建立α-突触核蛋白(α-synuclein,α-syn)聚集及传播的细胞和动物模型,为帕金森病的发病机制研究提供基础。方法 亲和层析法纯化α-syn蛋白,体外诱导其聚集成为α-syn纤维(Preformed fibrils,PFFs); 培养稳定表达GFP-α-syn的HEK293细胞系及原代神经元,转导α-synPFFs后免疫荧光染色法观察细胞内α-syn聚集情况; 小鼠立体定位注射α-syn PFFs,免疫组织化学法检测内源性α-syn的聚集及传播情况。结果 纯化的α-syn可在体外聚集形成聚集体; 在细胞及动物水平观察到α-syn PFFs可诱导内源性蛋白的聚集和传播。结论 本研究建立了α-syn聚集及传播的细胞和动物模型,为帕金森病的相关研究打下了基础。 相似文献
2.
目的探讨格尔德霉素(geldanamycin,GA)通过诱导热休克蛋白(HSP)反应抑制α-突触核蛋白(α-syn)异常表达,加强泛素蛋白酶体降解功能的神经保护作用。方法鱼藤酮作用于NGF诱导的PC12细胞建立α-syn胞质内过表达细胞模型,MTT法检测GA不同浓度及用药时程条件下的细胞活力,应用Western blot技术及共聚焦免疫荧光双标染色观察GA预处理后细胞内HSP70和α-syn的表达。荧光分光光度计测量各组细胞内蛋白酶体水解酶活性的变化。结果MTT示GA20~300nmol·L-1预处理使细胞活力呈浓度依赖性上升,吸光度分别上升至正常的65%、76%、85%和94%(鱼藤酮组为59%,P<0·01),而GA与鱼藤酮同时给药或作用于其后20h细胞活力无明显变化。Western blot结果提示GA预处理使HSP70表达上升至正常的3倍左右。共聚焦显微镜观察显示α-syn过表达现象得以抑制,并证实两者的共定位现象。酶活性测定提示GA预处理使类胰蛋白酶,类糜蛋白酶活性明显增强,荧光指数分别上升至10·4±1·61和96·0±4·77(鱼藤酮组为7·9±0·90和82·4±3·51,P<0·05),PgH水解酶活性也轻度上升。结论格尔德霉素可诱发热休克蛋白反应,主要通过HSP70的作用抑制α-syn的异常表达,促进泛素蛋白酶体降解功能,减轻蛋白水解应激反应,发挥神经保护效应。 相似文献
3.
计算机程序化的初均速法测定双黄连注射液的稳定性 总被引:2,自引:0,他引:2
用计算机程序化的初均速法,测定了双黄连溶液中3种主要成分——绿原酸、黄苓甙、连翘甙的活化能及室温贮存期。该方法简便、快速、结果准确。对临床应用有一定价值。 相似文献
4.
以FeCl3的甲醇溶液为显色剂,用标准曲线法在440nm检测吸收度,直接测定了培氟沙星注射液的含量,与高效液相色谱法所测试结果比较,平均标示量分别为105.4%和102.6%,二种方法所得结果无显著性差异。 相似文献
5.
贫血小儿肺炎时脂质过氧化作用及其临床分析徐锁全,张建清,张振涛,兰海霞,常桂琴(中国人民解放军第253医院,内蒙古医学院)在医学领域人们研究超氧化物阴离子自由基()对机体损害时发现贫血小儿活性氧产生下降[1],而对贫血小儿抵抗力降低及其合并感染时产生... 相似文献
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In order to study neurotransmitter receptor regulation in the basal ganglia involved in the functional changes underlying levodopa-induced motor complications, quantitative autoradiography was used to observe receptor bindings of dopamine D1 and D2, N-methyl-D-aspartate (NMDA), amino-3-hydroxy-5-methylisoxazole propionic acid (AMPA) and amino butyric acid (GABA) in the basal ganglia of rats that had unilateral nigrostriatal lesions and had been chronically treated with levodopa until motor complications developed. The rats were randomly assigned to three groups: normal, denervated and treatment-complicated groups. The results showed that response duration to levodopa became progressively shorter and abnormal involuntary movement (AIM) score was progressively increased during the course of levodopa treatment. Chronic treatment augmented D1 receptors more than denervation, and reduced D2 receptors that were also increased by dopamine denervation. Striatal NMDA receptors were substantially up-regulated in the treatment-complicated group. Levodopa treatment did not change receptors of nigral AMPA, pallidal GABA, and subthalamic GABA, which remained the same as that in denervation group. However, chronic treatment reversed the increase of nigral GABA receptors caused by the lesion. It was concluded that a shortening of response duration and AIM mimicked levodopa-induced motor complications of Parkinson's patients. These data suggested that up-regulation of dopamine D1 and NMDA receptors in the striatum leads to an imbalance of stimulation through the striatal output pathways, which is associated with levodopa-induced motor complications. 相似文献
8.
This study investigated the effect and mechanism of cell cycle reentry induced by 6-hydrodopamine (6-OHDA) in PC12 cells. By using neural differentiated PC12 cells treated with 6-OHDA, the apoptosis model of dopaminergic neurons was established. Cell viability was measured by MTT. Cell apoptosis and the distribution of cell cycle were assessed by flow cytometry. Western blot was used to detect the activation of extracellular regulator kinasel/2 (ERK1/2) pathway and the phosphorylation of retinoblastoma protein (RB). Our results showed that after PC12 cells were treated wtih 6-OHDA, the viability of PC12 cells was declined in a concentration-dependent manner. Flow cytornetry revealed that 6-OHDA could increase the apoptosis ratio of PC12 cells in a time-dependent manner. The percentage of ceils in G0/G1 phase of cell cycle was decreased and that in S phase and G2/M phase increased. Simultaneously, ERK1/2 pathway was activated and phosphorylated RB increased. It was concluded that 6-OHDA could induce cell cycle reentry of dopaminergic neurons through the activation of ERK1/2 pathway and RB phosphorylation. The aberrant cell cycle reentry contributes to the apoptosis of dopaminergic neurons. 相似文献
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张振涛 《中国中医药现代远程教育》2008,6(9)
痰饮既是病理产物,又是致病因素,作为病名,首见于《金匮要略》。痰饮有广义、狭义之分,历代医家对痰与饮有分论者。饮之生成,因外受之邪,内伤水饮,致脾胃运化失常,水饮停聚而成。痰之形成,因六淫侵袭者,或因其化热,煎熬津液致痰;或因其化痰,津液凝聚为痰。因内伤而致者,诸如饮食过伤,劳倦至极, 相似文献