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1.
目的 观察早期阿尔茨海默病 (AD)患者服用达纳康 (系法国银杏叶制剂 )治疗前后血浆生长抑素 (somatostatin ,SS)、精氨酸加压素 (argininevasopressin,AVP)、促肾上腺皮质激素 (corticotropin ,ACTH)及β内啡肽 (β endorphin ,β EP) 4种神经肽含量的影响。 方法 对 2 7例早期AD患者于达纳康治疗前后分别取血浆测定上述 4种神经肽含量 ,同时作简易智力状态检查 (MMSE)和韦氏成人智力量表 (中国修订 )(WAIS RC)测评 ,并与 30例正常老年人作对照。结果 AD组血浆AVP含量 (35.8± 1 9.2 4 )ng/L较对照组 (56.3± 2 0 .8)ng/L显著减少 (P <0 0 5) ;血浆SS、ACTH含量在治疗前分别为 (348.8± 2 1 0 .3)ng/L和 (8.2 5± 3 .85)ng/L ,治疗后则分别上升为 (881 .4± 363 .1 6)ng/L和 (1 9± 9.1 1 )ng/L。治疗前后比较均有非常显著性差异 (P <0 .0 0 1 )。AVP在治疗后血浆含量也有升高为 (57.85± 1 6 .86)ng/L,与治疗前比较有显著性差异(P <0 .0 5)。结论 早期AD患者血浆AVP含量减少 ,提示AVP可作为AD患者早期生化指标。早期AD患者在服用达纳康后SS、ACTH、AVP血浆含量均显著上升 ,提示SS、ACTH、AVP可能参与AD的发病机制  相似文献   

2.
目的 研究铅暴露大鼠海马神经细胞精氨酸加压素(AVP)、生长抑素(SS)的阳性表达,及其与学习记忆障碍的关系.方法 将健康两月龄SD大鼠60只,随机分为对照组、染铅组,每组30只,染铅动物饮用0.1%醋酸铅去离子水3个月,制成慢性染铅大鼠模型;对照组饮用去离子水.Y-迷宫试验检测两组大鼠的学习和记忆能力,采用免疫组化方法测定大鼠海马AVP和SS阳性神经元数,观察铅暴露对其阳性表达的影响.结果 染铅组大鼠学习记忆能力较对照组明显减低(P<0.01),海马CA1区AVP 和SS阳性神经元数量均明显减少(均P<0.01),CA3区AVP(P<0.05)和SS(P>0.05)阳性神经元数量亦减少,但不如CA1区明显.结论 铅暴露大鼠学习记忆能力的减低可能与海马神经细胞AVP和SS的阳性表达减少有关.  相似文献   

3.
目的 观察癫痫大鼠大脑皮质、海马糖皮质激素受体 (GR)的改变 ,阐明 GR在癫痫发生发展中的作用。方法 采用美解眠皮下注射方式建立大鼠癫痫模型。应用免疫组织化学 ABC法测定 60只 SD雄性大鼠大脑皮质及海马齿状回 GR阳性细胞数目的变化。结果 急性致癫痫组大鼠大脑皮质、海马齿状回 GR阳性细胞数显著低于对照组 (P <0 .0 0 1 ) ;慢性致癫痫组大鼠大脑皮质、海马齿状回 GR阳性细胞数显著高于对照组 (P <0 .0 1 )和急性致癫痫组 (P<0 .0 0 1 )。结论 大脑皮质和海马 GR水平的变化可能与癫痫发病有关。  相似文献   

4.
L—NA对大鼠学习记忆的影响及NO、SS相关性研究   总被引:5,自引:0,他引:5  
目的 探讨一氧化氮(NO)和生长抑素(SS)在学习记忆过程中的作用及相互作用。方法 大鼠海马微量注射一氧化氮合酶(NOS)抑制剂N-ω硝基-L精氨酸(N-ω-Nitro-L-Arginine,L-NA) 后采用Y型电迷宫观察大鼠学习记忆能力的改变,以硝酸还原酶法测定海马NO含量,以放射免疫法测定海马SS含量,并进行学习记忆能力、NO含量和SS含量相关性分析。结果 海马微量注射L-NA组大鼠与生理盐水对照组和正常对照组比较,海马中NO、SS含量明显下降(P<0.01)。Y型电迷宫测定次数明显增加(P<0.01),L-NA组大鼠海马NO水平和SS水平呈显著正相关,NO、SS水平均与Y型电迷宫测试次数呈显著负相关。结论 海马中NO、SS水平的正常是机体实现正常学习和记忆过程的重要因素;NO可能通过调节SS的合成和释放,共同促进学习和记忆过程。  相似文献   

5.
检测原发性癫痫患者和对照组血和脑脊液(CSF)中6种神经肽,血中5项免疫指标和催乳素(PRL)的含量,对三者之间的关系进行相关分析。结果显示,与对照组相比,癫痫组(1)血中亮氨酸脑啡肽(LEK)、强啡肽(Dyn)、精氨酸加压素(AVP)、神经降压素(NT)、生长抑素(SS)和PRL以及CSF中的LEK、AVP、NT和SS含量均显著增高;(2)血中NK细胞、ADCC、T淋巴细胞总花环形成率(TRF)、T淋巴细胞活性花环形成率(ARF)和总补体(CH50)含量均显著降低;(3)在神经肽、免疫指标和PRL三者中,有多项指标之间存在显著相关性。结果提示,神经内分泌免疫网络调节功能变化在原发性癫痫的发病机理中可能有一定地位。  相似文献   

6.
将老年大白鼠(24个月)左侧海马繖部分切断,建立基底前脑胆碱能损害的老年痴呆动物模型。予侧脑室注射神经生长因子(NGF),分别在用药后15天和30天测隔区和海马胆碱乙酰转移酶(ChAT)活性。以正常鼠组和细胞色素C注射组作为对照。损害后隔区和同侧海马ChAT活性显著减少;NGF15天治疗组,隔区和损害对侧海马酶活性显著增加,是正常组的130%;30天治疗组,同侧海马酶活性比细胞色素C组增加48%。结果表时,NGF对老年鼠基底前脑胆碱能系统损害的治疗是有效的。本文还讨论了NGF在损害后急、慢性期的作用机制。  相似文献   

7.
急性脑血管病下丘脑-垂体-肾上腺皮质轴变化的观察   总被引:4,自引:0,他引:4  
目的 观察急性脑血管病时下丘脑 垂体 肾上腺皮质轴的功能变化。方法 应用放射免疫方法检测急性脑血管病患者肾上腺皮质激素 (Cor) ,促肾上腺皮质激素 (ACTH)的含量。结果 急性脑血管病患者血清ACTH、Cor含量均高于对照组 ,差异有显著性 (P <0 .0 1) ,血清ACTH、Cor含量与脑损伤范围成正比 ,急性脑血管病恢复期血清ACTH、Cor含量明显低于急性期 ,有显著差异 (P <0 .0 1)。结论 急性脑血管病患者血清ACTH、Cor含量均有改变 ,是可逆的。  相似文献   

8.
目的 观察双侧海马同时点燃时 ,是因破坏了点燃的拮抗作用而加速达到痫性发作 ,还是因点燃的拮抗作用的增强而延缓达到痫性发作。方法 按照Goddard方法将 2 0只成年Warster兔的双侧海马同时点燃 ,并与单侧海马点燃组作对照。结果 双侧海马同时点燃组 (BK)所有兔在平均 31次刺激后均出现 5期惊厥 ,8只兔显示有自发性痫性放电。在点燃早期 ,后放电 (AD)持续时间突然增加 ,此后逐渐增加。与单侧点燃 (UK)动物相比 ,双侧点燃法能显著提高动物点燃的成功率 (10 0 %对 5 5 % ,P <0 .0 1) ,但也显著减缓了点燃的进程 (31天 / 2 0天 ,P <0 .0 1)。结论 BK方法表现为神经元兴奋和抑制机制都增强。BK对点燃的致痫机制和筛选抗惊厥药物研究提供了一种更先进的复杂部分性癫痫动物模型。  相似文献   

9.
戊四唑致癫痫大鼠脑组织NO5和MDA含量及其相关性研究   总被引:3,自引:0,他引:3  
目的 探讨一氧化氮 (NO)在戊四唑诱导癫痫中的作用机制。方法 用戊四唑建立大鼠癫痫模型 ,测定癫痫发作后和对照组大鼠大脑皮质、海马中 NO、丙二醛 (MDA)含量及 NO合酶 (NOS)活性。结果 癫痫发作后大脑皮质、海马中 NO、MDA含量及 NOS活性较对照组显著升高 (P<0 .0 5或 P<0 .0 1) ;NO与MDA、NO与 NOS之间呈显著正相关 (两者均 P<0 .0 1)。结论  NO通过增强脂质过氧化反应在癫痫发作中发挥重要作用  相似文献   

10.
阿尔茨海默病脑海马凋亡神经元发生率增高   总被引:4,自引:0,他引:4  
通过对阿尔茨海默病 (Alzheimer’sdisease ,AD)和老年对照患者死后脑海马凋亡神经元的检测 ,探讨AD脑神经元丢失的可能机制。使用TUNEL(terminaltransferase mediateddUTP biotinnickendlabeling)法对 7例确诊的AD和 9例老年对照患者死后海马组织中的凋亡神经元进行标记 ,用生物图像分析系统对结果进行定量分析。AD和对照组间TUNEL阳性细胞数无显著性差异 ;AD组海马CA1和CA4区正常神经元数减少 ,其中CA1区减少具有显著性差异 (P <0 .0 5 ) ;AD组海马CA1和CA4区凋亡神经元发生率高于对照组 ,其中CA1区具有显著性差异 (P <0 .0 5 )。AD组海马组织中凋亡神经元发生率明显增高 ,说明细胞凋亡可能参与了AD海马神经元退行性变的过程。  相似文献   

11.
Expression of mRNAs coding for the ACTH secretagogues corticotropin-releasing factor (CRF) and arginine vasopressin (AVP) was examined in the hypothalamic paraventricular nucleus (PVN) of rats bearing hippocampal lesions. Either total hippocampectomy (HPX) or extirpation of the dorsal hippocampus (DHPX) precipitated a 4-fold increase in CRF mRNA expression relative to sham-operated controls (SHAM), as determined by semiquantitative in situ hybridization histochemistry. AVP mRNA was localized to individual parvocellular neurons of the medial parvocellular division of the PVN in only the HPX and DHPX groups, consistent with enhanced production of AVP message in this neuronal population subsequent to hippocampal damage. HPX did not affect AVP mRNA content in magnocellular divisions of PVN. Plasma beta-endorphin levels were significantly elevated in the HPX and DHPX groups relative to SHAM animals, indicating a chronic increase in release of proopiomelanocortin peptides from the anterior pituitary gland in response to hippocampal lesion. Circulating corticosterone levels were elevated in HPX rats as well. To control for effects of lesion size and location, additional animals received large ablations of cerebral cortex or cerebellum. In neither case was CRF or AVP mRNA significantly altered in the PVN. The results suggest that the hippocampus exercises a tonic inhibitory role on ACTH secretagogue production in neuroendocrine neurons promoting ACTH release.  相似文献   

12.
目的:对脑缺血大鼠采用尼莫地平与石杉碱甲进行药物干预治疗,观察治疗后不同药物组血管内皮生长因子(VEGF)、caspase-3表达水平与学习记忆改善程度。方法:采用免疫组化和Y迷宫检测脑缺血鼠学习记忆功能的变化及VEGF、caspase-3在缺血区的表达。结果:各治疗组VEGF、caspase-3在海马区、大脑皮质、基底节区表达均显著低于脑缺血对照组(A组)P<0.01,尤以海马、大脑皮质区较显著。其中石杉碱甲加尼莫地平干预组(B组)VEGF、caspase-3细胞阳性表达的降低和学习记忆功能的改善,明显好于A、C、D组,P<0.01。结论:石杉碱甲加尼莫地平治疗组与其他药物治疗组比,能有效改善VEGF、caspase-3表达水平和提高学习记忆的能力,为认知障碍早期的治疗提供依据。  相似文献   

13.
BACKGROUND:Glossy privet fruit inhibits neural cell apoptosis following the onset of vascular dementia. OBJECTIVE:To confirm glossy privet fruit effects on neural cell apoptosis in the cortical parietal lobe and hippocampal CA1 region of rat models of vascular dementia using molecular biology techniques. DESIGN,TIME AND SETTING: The neural cell morphology experiment was performed at the Laboratory of Flow Cells and Biochemistry,Academy of Integrative Medicine,Fujian University of Traditional Chinese Medicin...  相似文献   

14.
目的观察胰岛素治疗对糖尿病大鼠学习记忆功能障碍及大脑皮层、海马内生长抑素(SS)、血管活性肠肽(VIP)含量变化的作用。方法采用链脲菌素制备雄性WiStar大鼠糖尿病模型,设正常对照组、胰岛素治疗糖尿病组、未治疗糖尿病组。3个月后采用T型水迷宫试验测定大鼠学习记忆功能,采用放免法测定皮层额叶、海马区脑组织SS、VIP含量。结果与正常对照组比较,未治疗糖尿病大鼠游迷宫时间显著延长、正确次数显著减少,额叶皮层、海马区脑组织SS含量显著降低,VIP含量无显著变化;胰岛素治疗组大鼠上述变化无显著意义。结论糖尿病引起大鼠学习记忆功能障碍和SS下降;SS下降与学习记忆功能障碍有关;早期胰岛素治疗可使学习记忆功能和SS含量恢复正常。  相似文献   

15.
Tiantai No. 1, a Chinese medicine predominantly composed of powderedRhizoma Gastrodiae,Radix Ginseng, and Ginkgo leaf at a ratio of 2:1:2 and dissolved in pure water, is neuroprotective in animal models of various cognitive disorders, but its molecular mechanism remains unclear. We administered Tiantai No. 1 intragastrically to senescence-accelerated mouse prone 8 (SAMP8) mice (a model of Alzheimer’s disease) at doses of 50, 100 or 150 mg/kg per day for 8 weeks and evaluated their behavior in the Morris water maze and expression of Alz-heimer’s disease-related proteins in the brain. Tiantai No. 1 shortened the escape latency in the water maze training trials, and increased swimming time in the target quadrant during the spatial probe test, indicating that Tiantai No. 1 improved learning and memory in SAMP8 mice. Immunohistochemistry revealed that Tiantai No. 1 restored the proliferation potential of Ki67-positive cells in the hippo-campus. In addition, mice that had received Tiantai No. 1 had fewer astrocytes, and less accumulation of amyloid-beta and phosphorylated tau. hTese results suggest that Tiantai No. 1 is neuroprotective in the SAMP8 mouse model of Alzheimer’s disease and acts by restoring neuronal number and proliferation potential in the hippocampus, decreasing astrocyte inifltration, and reducing the accumulation of amy-loid-beta and phosphorylated tau.  相似文献   

16.
BACKGROUND: Previous research has revealed that somatostatin can induce epilepsy, and that the levels of neuropeptide Y may increase and become more active in brain areas with epileptic seizures.OBJECTIVE: To observe the effect of Ganoderma lucidum spore powder on the neuropeptide Y and somatostatin content in the cerebral cortex and hippocampal regions of seizure rats induced by pentylenetetrazol (PTZ). Furthermore, to verify any effect of Ganoderma lucidum spore powder on inhibition of epileptic seizures.DESIGN, TIME AND SETTING: A randomized group animal study was performed in August 2007 in the School of Basic Medical Sciences, Jiamusi University (Jiamusi, Heilongjiang, China).MATERIALS: Thirty healthy, male, Wistar rats, aged 12 weeks and weighing 180-220g, were taken as the experimental animals. PTZ (Sigma Company, United States) was used to induce epilepsy. Ganoderma lucidum spores (Leyss, ex Fr variety) were purchased from Jiamusi City Wild Growing Case of the Ganoderma Lucidum (China). Rabbit anti-somatostatin antibodies and secondary antibodies were purchased from Wuhan Boster Company (China). Neuropeptide Y radioimmunoassay kit was purchased from Beijing Furui Biotechnology Company (China).METHODS: Thirty rats were randomly divided into three groups: a control group, an epilepsy model group and a Ganoderma lucidum spore-treated group. Each group contained 10 animals. Rats in the epilepsy model group were treated with intraperitoneal injections of PTZ and gastric perfusion of physiologic saline, In the Ganoderma lucidum spore-treated group, intraperitoneal injection of PTZ and gastric perfusion of Ganoderma lucidum spore powder were administered. The blank control group was only administered with the physiological saline by intraperitoneal injection and gastric perfusion.MAIN OUTCOME MEASURES: Immunohistochemical staining and radioimmunoassay methods were used to observe the changes of somatostatin and neuropeptide Y content in brain tissue of epileptic rats, as well as the morphology of neurons.RESULTS: All 30 rats were involved in the result analysis, without any loss. The number of somatostatin immunoreacted positive cells in the cerebral cortex and hippocampus was significantly increased in the epilepsy model group compared to the blank control group (P<0.01). The number of somatostatin immunoreacted positive cells in cerebral cortex and hippocampus was significantly decreased in the Ganoderma lucidum spore-treated group compared to the epilepsy model group (P<0.01). The contents of neuropeptide Y in cerebral cortex and hippocampus were significantly increased in the epilepsy model group compared to the blank control group (P<0.01). The contents of neuropeptide Y in the cerebral cortex and hippocampus were significantly decreased in the Ganoderma lucidum spore-treated group compared to the epilepsy model group (P<0.05). The epilepsy seizures in the Ganoderma lucidum spore-treated group were obviously reduced compared to the epilepsy model group.CONCLUSION: Ganoderma lucidum spore powder was able to reduce the somatostatin and neuropeptide Y content in the cerebral cortex and hippocampus effectively, so as to achieve an anti-epileptic function and protect neurons from being damaged.  相似文献   

17.
目的:探讨精氨酸加压素(AVP)的功能变化在抑郁症发生中的作用. 方法:应用化学发光免疫分析法和酶联免疫法测定83例抑郁症患者、57例正常对照者的血浆促肾上腺皮质激素(ACTH)、AVP和皮质醇(Cor)浓度水平. 结果:抑郁症组血浆ACTH浓度(48±30) ng/L、Cor浓度( 188±59) μg/L分别高于正常对照组(18 ±7) ng/L、( 165±55)μg/L,差异有统计学意义(t=9.422,P<0.01;t =2.453,P<0.05);抑郁症组血浆AVP浓度(6.0±5.7) ng/L与对照组(4.5±2.6) ng/L差异无统计学意义(t=1.849,P<0.05).ACTH异常的(ACTH≥50ng/L)抑郁症患者AVP、Cor浓度[(8.0±7.0)ng/L,(211±55) μg/L]高于ACTH正常的(ACTH< 50 ng/L)抑郁症患者[(3.5±3.2) ng/ml,( 174±58)μg/L],差异有统计学意义(t=2.728,t =3.027,P均<0.01).抑郁症患者的AVP与ACTH存在正相关(r=0.286,P=0.027),ACTH与Cor存在正相关(r=0.455,P=0.000). 结论:ACTH水平增高的抑郁症患者AVP异常,AVP调节功能可能是影响抑郁症疾病过程的一个因素.  相似文献   

18.
应用大鼠急性脑缺血再灌注动物模型,观察精氨酸加压素(AVP)在急性脑缺血再灌注损伤中的变化及与脑水肿关系,结果表明丘脑下部AVP含量在脑缺血30min明显增加,再灌注60min后进一步增加,且与大脑皮层水含量是显著相关性。提示,AVP参与急性脑缺血再灌注损伤,丘脑下部AVP含量增高,可加重或促进脑缺血再灌注后脑水肿形成。  相似文献   

19.
Brain edema formation is one of the most important mechanisms of ischemia-evoked cerebral edema. It has been demonstrated that arginine vasopressin (AVP) receptors are involved in the pathophysiology of secondary brain damage after focal cerebral ischemia. In a well-characterized animal model of ischemic stroke of Mongolian gerbils, the present study was undertaken to clear the effect of AVP on cortex edema in cerebral ischemia. The results showed that (1) occluding the left carotid artery of Mongolian gerbils not only decreased the cortex specific gravity (cortex edema) but also increased AVP levels in the ipsilateral cortex (ischemic area) including left prefrontal lobe, left parietal lobe, left temporal lobe, left occipital lobe and left hippocampus for the first 6 hours, and did not change of the cortex specific gravity and AVP concentration in the right cortex (non-ischemic area); (2) there were many negative relationships between the specific gravity and AVP levels in the ischemic cortex; (3) intranasal AVP (50 ng or 200 ng), which could pass through the blood–brain barrier to the brain, aggravated the focal cortex edema, whereas intranasal AVP receptor antagonist-D(CH2)5Tyr(ET)DAVP (2 µg) mitigated the cortex edema in the ischemic area after occluding the left carotid artery of Mongolian gerbils; and (4) either intranasal AVP or AVP receptor antagonist did not evoke that edema in the non-ischemic cortex. The data indicated that AVP participated in the process of ischemia-evoked cortex edema, and the cerebral AVP receptor might serve as an important therapeutic target for the ischemia-evoked cortex edema.  相似文献   

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