养血清脑颗粒对慢性脑供血不足患者临床疗效和血流动力学的影响

目的 观察养血清脑颗粒对慢性脑供血不足(CCCI)患者的临床疗效及对血流动力学的影响.方法 90例CCCI患者按就诊时间顺序分为对照组(A组)、养血清脑颗粒组(B组)、联合用药组(C组)各30例.于治疗前后分别检测患者血流动力学指标,同时选取健康志愿者30名为正常时照组,并统计分析.结果 B组、C组总有效率分别为90.00%和93.33%,与A组比较差异有统计学意义(P<0.05).治疗前A组、B组、C组平均血流速度与正常时照组比较有统计学意义(P<0.05).B组、C两组治疗后平均血流速度与治疗前比较差异均有统计学意义(P<0.05),与正常对照组比较差异无统计学意义(P>0.05).A组治疗后平均血流速度与治疗前以及与正常对照组比较个别项目差异有统计学意义.B组、C两组治疗后平均血流速度比较差异无统计学意义(P>0.05).结论 养血清脑颗粒能明显改善患者的血流动力学指标,增加脑供血,改善头晕、头痛等症状,单用齐血清脑颗粒治疗CCCI能达到满意的疗效.     

竹黄颗粒剂II号对银屑病患者外周血单个核细胞转录因子T-bet/GATA3 mRNA表达的影响

目的:探讨竹黄颗粒剂II号对寻常型银屑病的作用机制。方法:36例寻常型银屑病患者,按随机数字表,分竹黄颗粒剂II号治疗组(竹黄组)19例与银屑灵冲剂治疗组(银屑组)17例,分别于治疗前、后用RT-PCR技术检测外周血单个核细胞转录因子T-bet/GATA3 mRNA的表达,并以15例正常人作为对照组。结果:治疗后T-bet/GATA3 mRNA表达均显著改变(P<0.05);其中竹黄组效果优于银屑组(P<0.01)。结论:竹黄颗粒剂II号治疗银屑病有效的机制可能是通过降低患者T-bet/GATA3 mRNA的表达。     

Cannabinoids inhibit hippocampal GABAergic transmission and network oscillations

Using a new antibody developed against the C-terminus of the cannabinoid receptor (CB1), the immunostaining in the hippocampus revealed additional axon terminals relative to the pattern reported previously with an N-terminus antibody. Due to a greater sensitivity of this antibody, a large proportion of boutons in the dendritic layers displaying symmetrical (GABAergic) synapses were also strongly immunoreactive for CB1 receptors, as were axon terminals of perisomatic inhibitory cells containing cholecystokinin. Asymmetrical (glutamatergic) synapses, however, were always negative for CB1. To investigate the effect of presynaptic CB1 receptor activation on hippocampal inhibition, we recorded inhibitory postsynaptic currents (IPSCs) from principal cells. Bath application of CB1 receptor agonists (WIN55,212-2 and CP55,940) suppressed IPSCs evoked by local electrical stimulation, which could be prevented or reversed by the CB1 receptor antagonist SR141716A. Action potential-driven IPSCs, evoked by pharmacological stimulation of a subset of interneurons, were also decreased by CB1 receptor activation. We also examined the effects of CB1 receptor agonists on Ca2+-independent miniature IPSCs (mIPSC). Both agonists were without significant effect on the frequency or amplitude of mIPSCs. Synchronous gamma oscillations induced by kainic acid in the CA3 region of hippocampal slices were reversibly reduced in amplitude by the CB1 receptor agonist CP 55,940, which is consistent with an action on IPSCs. We used CB1-/- knock-out mice to confirm the specificity of the antibody and of the agonist (WIN55,212-2) action. We conclude that activation of presynaptic CB1 receptors decreases Ca2+-dependent GABA release, and thereby reduces the power of hippocampal network oscillations.     

Morphological evidence for altered synaptic organization and structure in the hippocampal formation of seizure-sensitive gerbils.

Seizure-sensitive (SS) and seizure-resistant (SR) Mongolian gerbils were used for three experiments. In the first experiment, GABAergic neurons and terminals in the dentate gyrus were localized with GAD immunocytochemistry. GAD-positive puncta adjacent to cell bodies of GABAergic pyramidal basket cells were counted in light microscopic preparations. The pyramidal basket cells of SS gerbils displayed a significant threefold increase in the number of GAD-positive puncta associated with their cell bodies as compared to those from SR gerbils. These data indicate that the number of GABAergic synapses with pyramidal basket cell bodies in the dentate gyrus was greater in SS gerbils. An electron microscopic (EM) analysis of GAD immunocytochemical preparations showed GAD-positive axon terminals forming symmetric synapses with GAD-positive basket cell bodies. However, numerous terminals forming symmetric axosomatic synapses with basket cells were not immunopositive, and other synapses formed by terminals were not classified because reaction product in the cell bodies obscured postsynaptic densities. Therefore, routine EM preparations were analyzed for symmetric and asymmetric axosomatic synapses on pyramidal basket cells and granule cells of SS and SR gerbils. The data obtained from these preparations showed that the pyramidal basket cells of SS gerbils had a selective increase in the number of symmetric synapses per 10 microns of soma as compared to those of the SR gerbils. In contrast, the granule cells did not show any significant difference in the number of either symmetric or asymmetric axosomatic synapses between SS and SR gerbils. These results indicate that pyramidal basket cell bodies of SS gerbils have more inhibitory synapses than do those of SR gerbils. The third experiment used SS gerbils with lesions of the perforant pathway that stopped seizure activity (Ribak, C. E., and S. U. Khan (1987) The effects of knife cuts of hippocampal pathways on epileptic activity in the seizure-sensitive gerbil. Brain Res. 418:251-260). The percentage of axon terminal area occupied by synaptic vesicles and their packing density was determined in CA3 mossy fiber boutons and compared for lesioned and nonlesioned SS gerbils. The mossy fibers of nonlesioned SS gerbils showed a depletion of synaptic vesicles consistent with the previous results of Peterson et al. (Peterson, G. M., C. E. Ribak, and W. H. Oertel (1985) A regional increase in the number of hippocampal GABAergic neurons and terminals in the seizure-sensitive gerbil. Brain Res. 340:384-389).(ABSTRACT TRUNCATED AT 400 WORDS)     

提取-共沸精馏耦合工艺提取挥发油制备颈复康颗粒的活血化瘀作用

目的:研究提取-共沸精馏耦合工艺(water extraction coupling rectification,WER)提取挥发油制备颈复康颗粒对实验性体内、外血栓形成、血液黏度及脑血流量的影响,对WER工艺制备的颈复康颗粒进行药理学评价。方法:取SD大鼠40只,随机分成5组,每组8只。即颈复康颗粒高、低剂量组(12,6 g.kg-1)、WER工艺颈复康颗粒高、低剂量组(12,6 g.kg-1)及空白对照组,各组连续ig给药7 d。大鼠体外血栓形成:末次给药后2 h,自腹腔动脉取血,置体外血栓形成仪上测量血栓长度、湿重、干重;大鼠体内血栓形成:末次给药后2 h麻醉大鼠,分离颈总动脉,观察记录体内血栓形成时间;自腹腔静脉取血测定大鼠血小板聚集率、高切、中切、低切下全血黏度及血浆黏度;取健康成年家犬30只,分组及给药等同前,观察记录用药前后家犬脑血流量(cerebral blood flow,CBF)及脑血管阻力(cerebral vascular resistance,CVR),分析WER工艺与传统工艺制备的颈复康颗粒对上述各项指标的影响。结果:WER工艺提取挥发油制备的颈复康颗粒高、低剂量组均可显著延缓大鼠血栓形成时间(OT延长率为33.34%,18.87%),降低大鼠体外血栓长度、湿重和干重,降低血小板聚集率及全血黏度和血浆黏度(血小板5min聚集阻抗值分别为6.15Ω,7.24Ω),在末次给药后30～90 min均可增加家犬脑血流量,且与传统工艺颈复康颗粒同剂量组比较差异有显著性。结论:WER工艺提取挥发油制备的颈复康颗粒较传统工艺制备的颈复康颗粒具有更好的活血化瘀作用。     

小青龙汤配方颗粒与传统饮片中芍药苷含量的比较

目的 比较小青龙汤配方颗粒与传统饮片中芍药苷的含量。方法 采用高效液相色谱法进行分析比较研究。结果 该测定方法精密度、稳定性和重复性良好，平均回收率为101．78％，RSD=0．85％。结论 两种剂型中芍药苷的含量无明显差异。     

辛芩颗粒药效学研究

目的：研究辛芩颗粒对过敏性介质组织胺的对抗作用。方法：豚鼠口服辛芩颗粒剂一次后1．5h,用2％组织胺溶液超声雾化法引喘30s,记录动物呼吸困难和窒息抽搐出现的潜伏时;大鼠口服辛芩颗粒剂3d后,背部皮内注射1％组织胺溶液0．1ml/点,两点／只,立即尾静脉注射1％伊文思蓝0．5ml/100g,15min后放血处死动物,测定背部注射点染料渗出量。结果：3．2053g生药／kg对组织胺性哮喘即有抑制作用,1．602g生药／kg对组织胺性色素渗出已有抑制作用,并均与剂量有关。结论：辛芩颗粒对过敏性介质组织胺有确定的对抗作用。     

稳心颗粒联合尼可地尔治疗缺血性心肌病房性心律失常临床观察

目的探讨缺血性心肌病伴房性心律失常采用稳心颗粒联合尼可地尔治疗的临床效果。方法选择2017年1月—2019年1月收治的缺血性心肌病伴房性心律失常患者114例,遵照不同治疗原则分组标准分为对照组和研究组,各57例,2组入院后均采用常规基础治疗,对照组在基础治疗的基础上给予稳心颗粒进行治疗。研究组在对照组的基础上联合应用尼可地尔进行治疗,比较2组治疗效果、心功能情况、P波离散程度、6 min步行试验距离以及不良反应。结果研究组治疗总有效率为96.49%,显著高于对照组(80.70%),差异有显著性意义(P<0.05)。研究组心功能、P波离散程度、6 min步行距离以及脑钠素水平均显著好于对照组,差异均存在统计学意义(P<0.05),但2组患者用药后不良反应发生率比较,差异无统计学意义(P>0.05)。结论稳心颗粒联合尼可地尔应用于缺血性心肌病伴房性心律失常患者的治疗中,能够显著提高治疗效果,改善心脏功能,且未见明显不良反应,好于单一用药,值得推广。     

Cerebellar cortical-layer-specific control of neuronal migration by pituitary adenylate cyclase-activating polypeptide

Migration of immature neurons is essential for forming the cortical layers and nuclei. Impairment of migration results in aberrant neuronal cytoarchitecture, which leads to various neurological disorders. Neurons alter the mode, tempo and rate of migration when they translocate through different cortical layers, but little is known about the mechanisms underlying this process. Here we show that endogenous pituitary adenylate cyclase-activating polypeptide (PACAP) has short-term and cortical-layer-specific effects on granule cell migration in the early postnatal mouse cerebellum. Application of exogenous PACAP significantly slowed the migration of isolated granule cells and shortened the leading process in the microexplant cultures of the postnatal day (P)0-3 cerebella. Interestingly, in the cerebellar slices of P10 mice, application of exogenous PACAP significantly inhibited granule cell migration in the external granular layer (EGL) and molecular layer (ML), but failed to alter the movement in the Purkinje cell layer (PCL) and internal granular layer (IGL). In contrast, application of PACAP antagonist accelerated granule cell migration in the PCL, but did not change the movement in the EGL, ML and IGL. Inhibition of the cAMP signaling and the activity of phospholipase C significantly reduced the effects of exogenous PACAP on granule cell migration. The PACAP action on granule cell migration was transient, and lasted for approximately 2 h. The duration of PACAP action on granule cell migration was determined by the desensitization of its receptors and prolonged by inhibiting the protein kinase C. Endogenous PACAP was present sporadically in the bottom of the ML, intensively in the PCL, and throughout the IGL. Collectively, these results indicated that PACAP acts on granule cell migration as "a brake (stop signal) for cell movement." Furthermore, these results suggest that endogenous PACAP slows granule cell migration when the cells enter the PACAP-rich PCL, and 2 h later the desensitization of PACAP receptors allows the cells to accelerate the rate of migration and to actively move within the PACAP-rich IGL. Therefore, endogenous PACAP may provide a cue that regulates granule cell migration in a cerebellar cortical-layer-specific manner.