醒脑健神胶囊对家兔脑血肿及血脑屏障影响的实验研究

利用自体血凝块颅内埋藏法复制家兔脑血肿模型，在造模后不同时间测定血气值、脑组织水、伊文斯蓝（ＥＢ）、脑指数及病理形态学方面的改变。结果显示：脑血肿形成后，动物有过度通气，脑组织含水量、脑指数明显增加，血脑屏障（ＢＢＢ）受损，通透性增强，有ＥＢ透过ＢＢＢ。选用醒脑健神胶囊进行治疗，能显著改善通气异常，降低ＢＢＢ通透性，减轻脑组织蓝染范围与程度，促进脑组织内血肿的吸收，对脑水肿的防治和ＢＢＢ的保护有明显的作用。     

聪圣胶囊对智力低下大鼠海马CA1区氨基酸含量的影响

目的　观察脑反复缺血再灌注后智力低下大鼠海马ＣＡ１ 区氨基酸含量及用“聪圣胶囊”治疗后的变化。方法　反复夹闭双侧颈总动脉制成智力低下大鼠,分别于术后１ｄ、７ｄ、１５ｄ、３０ｄ 检测海马ＣＡ１ 区氨基酸含量。结果　模型组氨基酸含量出现了先增加后减少的显著改变;用“聪圣胶囊”干预组的氨基酸含量亦有波动,但较模型组明显减轻;假手术组的含量无变化。结论　“聪圣胶囊”对神经细胞具有一定的保护作用。     

氯沙坦对卒中易感型自发性高血压大鼠的脑保护作用

目的 研究氯沙坦对卒中易感型自发性高血压大鼠(SHRsp)脑保护作用的机制。方法 6周龄雄性SHRsp随机分为生理盐水组、小剂量氯沙坦组(10mg·kg-1·d-1)和大剂量氯沙坦组(30mg·kg-1·d-1),记录血压和脑卒中临床表现评分,18周后处死,光镜观察脑卒中的发生率和脑血管结构;电镜观察脑组织的超微结构;TUNEL法检测神经细胞凋亡。结果 大剂量氯沙坦组血压明显低于未用药组(PO.05)。对照组SHRsp死亡率、脑动脉中膜厚度/管腔半径的比值和神经细胞凋亡率均高于小剂量和大剂量氯沙坦组,差异均有显著性意义(P相似文献   

托吡酯对癫痫大鼠海马细胞外液氨基酸和神经元凋亡的影响

目的研究托吡酯对癫癎大鼠海马区细胞外液氨基酸和神经元凋亡的影响.方法采用戊四氮(PTZ)致癎模型,大鼠癫癎发作后连续给予托吡酯(TPM)80 mg·kg-1·d-1和卡马西平40 mg·kg-1·d-1,共14 d.以TUNEL方法标记DNA片段,原位检测海马凋亡的神经细胞.脑内微透析技术采集大鼠海马细胞外液,反相高效液相色谱技术测定氨基酸类神经递质的含量.结果TPM组、卡马西平组与对照组比较,凋亡细胞数存在显著差异(P＜0.001),TPM组与卡马西平组相比无显著差异(P＞0.05).TPM可明显升高海马细胞外液γ-氨基丁酸(GABA)水平,并降低谷氨酸(Glu)浓度.结论TPM可减轻大鼠癫癎发作后的神经元损伤,这种作用可能是氨基酸变化的结果;但在我们的实验中,没有发现TPM对癫癎后脑损伤比卡马西平有更明显的神经保护作用.     

The effects of poststroke captopril and losartan treatment on cerebral blood flow autoregulation in SHRsp with hemorrhagic stroke

The ability of captopril and losartan treatment to restore cerebral blood flow (CBF) autoregulation after intracerebral hemorrhagic stroke (HS) was assessed in Kyoto–Wistar stroke-prone hypertensive rats (SHRsp). Laser Doppler techniques assessed CBF autoregulation in the middle cerebral artery (MCA) perfusion domain and a pressure myograph was used to measure pressure-dependent constriction (PDC) in isolated MCAs before and after stroke and after 13, 33, and 63 days of poststroke captopril or losartan treatment. The treatments did not lower blood pressure (BP) and equally suppressed plasma aldosterone after HS. The HS development was associated with the loss of CBF autoregulation, high CBF, increased CBF conductance to elevations in BP, and the loss of PDC in the MCAs. Both treatments restored these functions to prestroke levels within 13 days. The PDC and CBF autoregulation subsequently deteriorated after 63 days of captopril treatment while being maintained at prestroke levels over all durations of losartan treatment. The SHRsp subjected to 35 days of poststroke losartan treatment exhibited less blood–brain barrier (BBB) disruption and brain herniation than captopril-treated SHRsp. The superior ability of losartan to restore CBF autoregulation and myogenic function may have contributed to the more effective attenuation of cerebral damage after HS.     

Effect of atmospheric ions on hippocampal pyramidal neuron responsiveness to serotonin

The effect of long-term exposure to positive or negative atmospheric ions on the responsiveness of rat forebrain neurons to serotonin (5-HT) was studied. Male Sprague-Dawley rats were exposed to positive or negative ions (1.5 X 10(6) ions/ml) for 21 days, and a third group of rats served as controls. Unitary extracellular recordings from pyramidal neurons of the CA1 and CA3 regions of the dorsal hippocampus were obtained under urethane anesthesia, and their responsiveness to microiontophoretically applied acetylcholine (ACh), norepinephrine (NE) and 5-HT was assessed. Spontaneous rate of discharge and sensitivity to NE and ACh of hippocampal neurons were not affected by exposure to atmospheric ions. Exposure to negative ions increased and that to positive ions decreased the responsiveness of these neurons to 5-HT. During the winter, a circadian rhythm of responsiveness to 5-HT was observed in the control group, sensitivity being lowest in the morning and highest in the evening. Exposure to ions disrupted this circadian rhythm; in rats exposed to negative ions, responsiveness throughout the day was similar to that observed in the evening in the controls, whereas in rats exposed to positive ions, the circadian rhythm of responsiveness to 5-HT was inverted. Brain concentrations of 5-HT, tryptophan, and 5-hydroxyindoleacetic acid were unchanged by exposure to atmospheric ions.     

神经元兴奋性毒性对Munc18-1蛋白在大鼠海马神经元和原代培养神经元胞核内分布的影响(英文)

目的 Munc18-1在中枢神经系统递质释放过程中具有重要作用,控制着突触囊泡释放步骤的每一个环节。Munc18-1功能异常与癫痫发病相关。本文主要探讨癫痫是否会引起神经元胞核内Munc18-1定位的改变。方法通过海马内注射海人藻酸建立Sprague-Dawley(SD)大鼠癫痫模型,腹腔注射海人藻酸建立昆明小鼠癫痫模型。分离胎龄18天SD大鼠海马神经元,用Neurobasal培养基培养7天后,用谷氨酸处理3h。用蔗糖密度梯度离心法分离神经元和神经胶质细胞的细胞核组份,通过甲酚紫染色对上述富含细胞核的组份进行形态学鉴别。用免疫组化和免疫电镜分析法确定Munc18-1的细胞核定位。免疫印迹法检测不同细胞组分的Munc18-1蛋白的表达水平。结果免疫组化、免疫电镜以及对神经元细胞核组份的免疫印迹证实了Munc18-1在海马神经元细胞核的分布定位。在海人藻酸诱导癫痫的动物海马内,免疫组化染色显示Munc18-1在海马CA区锥体细胞层、齿状回颗粒细胞层和门区的多型细胞表达减少。同时,免疫印迹分析表明,Munc18-1在海马神经元胞核中的表达水平明显下降。免疫印迹检测显示,原代培养神经元经50μmol/L谷氨酸处理3h...     

Dickkopf-1在脑出血大鼠神经元凋亡中的作用及机制研究

目的探讨Dickkopf-1(DKK-1)在脑出血大鼠神经元凋亡中的作用及机制。方法采用随机数字法将40只成年雄性SD大鼠分成对照组(n=13)、假手术组(n=13)及脑出血组(n=14)。通过颅内注射自体外周血制作脑出血模型。采用平衡木行走实验和肌力测验进行脑出血模型评估,并利用Real-time PCR和Western blot检测大鼠脑组织中Bcl-2、Bax、p-Akt、Akt及DKK-1蛋白和mRNA表达水平。分离培养原代大鼠皮质神经元,分为对照组、空载体组、DKK-1过表达组、BTBD10(Akt磷酸化激活剂)过表达组,检测细胞中DKK-1表达水平和Akt磷酸化水平,利用流式细胞术检测各组细胞凋亡。结果脑出血组大鼠平衡木行走得分高于对照组和假手术组(P0.05),而肌力测验评分低于对照组和假手术组(P0.05)。与对照组和假手术组比较,大鼠脑出血部位脑组织Bcl-2表达降低(P0.05),而Bax表达则升高(P0.05),p-Akt表达水平下降(P0.05),DKK-1表达水平上升(P0.05)。DKK-1过表达组神经元凋亡率及p-Akt表达水平均高于空载体组和对照组(均P0.05)。Akt磷酸化激活剂BTBD10过表达组p-Akt水平、Bcl-2蛋白表达高于对照组和空载体组,而Bax蛋白表达则低于对照组和空载体组。BTBD10过表达组神经元存活率高于对照组和空载体组(均P0.05),且BTBD10和DKK-1共转染组大鼠神经元存活率高于DKK-1转染组(P0.05)。结论 DKK-1可能通过抑制Akt的磷酸化促进出血性脑卒中大鼠神经元的凋亡。     

出血性卒中与缺血性卒中危险因素比较

目的探讨不同危险因素对缺血性和出血性卒中发病的影响。方法收集3 102例脑卒中患者的个人疾病史、生活方式、临床检查及生化指标结果等资料,运用Epidata软件建立数据库,采用SAS 9.2进行统计分析。结果脑梗死组发病到入院时间、住院时间、高胆固醇血症、糖尿病史、心脏病史、房颤史、脑卒中史,吸烟的OR值分别是3.36、4.953、3.375、2.224、2.394、2.362、3.573、2.076、2.885。脑出血组呼吸、体温、心率、血压、高血糖、Tbil、高血压史OR值分别是0.824、0.390、0.673、0.425、0.594、0.598、0.934。结论发病到入院时间、住院时间、高胆固醇血症、糖尿病史、心脏病史、房颤史、脑卒中史、吸烟等对脑梗死的影响更大,而呼吸、体温、心率、高血压、高血糖、Tbil、高血压史对脑出血的影响更大。