白介素-6抗N-甲基-D-天门冬氨酸神经毒性作用的研究

目的:利用N-甲基-D-天门冬氨酸(NMDA)损伤小脑颗粒神经元的模型,探讨IL-6对神经损伤的保护作用,为临床上应用细胞因子防治脑损伤提供新思路。方法:取出生后8天幼鼠小脑的颗粒神经元做体外培养。用IL-6(10 ng/m l)慢性预处理培养的小脑颗粒神经元,孵育8天后用NMDA(10、100、1000和10000μmol/L)急性刺激小脑颗粒神经元30 m in以造成神经元损伤。用CCK-8试剂盒(Cell Counting K it-8)检测神经元的活性。结果:NMDA能呈浓度依赖性地抑制小脑颗粒神经元的活性。单纯IL-6慢性预处理小脑颗粒神经元,不能改变小脑颗粒神经元的活性。IL-6慢性预处理小脑颗粒神经元可明显改善NMDA对小脑颗粒神经元活性的抑制作用。结论:NMDA对神经元有浓度依赖性的神经毒性作用,IL-6具有抗NMDA神经毒性作用的效应。     

冠心病病人血浆vWF、GMP-140及Fg变化的临床分析

目的：探讨冠心病（CHD）病人血浆vWF、GMP-140及Fg在CHD发痛中的作用。方法：将CHD病人分为3组，观察各组血浆vWF、GMP-140及Fg的含量，与对照组比较。培果：CHD病人血浆vWF、GMP-140厦Fg与对照组比较有显著性差异（P＜0．05）；AMI上述指标明显增高（P＜0．01）。结论：CHD存在明显的高凝状态，vWF、GMP-140及Fg可预：则血栓形成的危险性。     

艾灵颗粒治疗国内HIV/AIDS患者104例临床研究

目的:观察艾灵颗粒治疗HIV/AIDS患者疗效.方法:选择符合HIV/AIDS诊断标准的患者,服用艾灵颗粒,30 d复诊1次,服用90 d为1疗程,观察2个疗程.做免疫功能、病毒载量变化的检查以及血象变化比较.结果:104例中,有效30例,稳定43例,无效31例,改善率70.19%.结论:艾灵颗粒具有一定程度上抑制HIV的复制,显示中药治疗艾滋病有较好的前景.     

颈性眩晕的针灸与养血清脑颗粒治疗

目的 探讨针灸与养血清脑颗粒治疗颈性眩晕的临床疗效。方法 选择诊断明确的颈性眩晕患者病例，随机分为两组，治疗组予以针灸治疗结束后口服养血清脑颗粒。对照组仅采用口服养血清脑颗粒。结果治疗组经颅多普勒超声检查椎基底动脉血流改善明显优于对照组（P〈0．05），治疗组自觉症状消失时间明显比对照组时间缩短（P〈0．01），随访半年、复发率明显优于对照组（P〈0．01）。结论 针灸与养血清脑颗粒治疗颈性眩晕可以明显提高疗效。     

眼络通颗粒的提取工艺研究

目的:研究眼络通颗粒的提取工艺。方法:采用正交设计试验,以葛根中葛根素转移率为指标,考察乙醇浓度、溶剂倍数、提取时间、提取次数对葛根乙醇提取效率的影响;采用水蒸气蒸馏法提取川芎、三棱中的挥发油,并制成β-环糊精包合物;采用水煎煮法提取其它药材中的水溶性成分。结果:葛根的最佳提取条件为取葛根药材8倍量的70%乙醇浸泡75min,再加热回流提取3次,每次2h;挥发油β-环糊精包合物制备方法为取15倍处方量川芎、三棱药材,加10倍量水,水蒸气蒸馏提取4h,用β-环糊精15g进行包合。结论:本工艺条件能最大限度提取药材中的有效成分。     

肝宁颗粒的质量标准研究

目的:建立肝宁颗粒的质量标准。方法:采用薄层色谱法对方中君药川芎进行定性鉴别,以高效液相色谱法测定川芎中阿魏酸的含量。结果:供试品色谱中,在与川芎对照药材相应的位置上,显相同颜色的荧光斑点;阿魏酸进样量在0·0384μg~0·2304μg范围内与峰面积积分值线性关系良好(r=0·9999),平均加样回收率为100·1%(RSD=0·91%)。结论:建立的质量标准可有效控制肝宁颗粒的质量。     

宫宁颗粒质量标准研究

目的:建立宫宁颗粒的质量标准。方法:采用薄层色谱法对宫宁颗粒中的黄芩苷进行定性鉴别;以高效液相色谱法测定黄芩苷的含量。结果:供试品薄层色谱中,在与黄芩苷对照品相应的位置上显相同颜色的斑点;黄芩苷检测浓度在20～100μg/ml范围内与峰面积积分值线性关系良好,平均回收率为99.71%(RSD=1.23%)。结论:所建质量标准可用于本品的质量控制。     

Selective and AMPA receptor-dependent astrocyte death following prolonged blockade of glutamate reuptake in rat cerebellar cultures

In this study we examined the effects of prolonged l-trans-pyrrolidine-2,4-dicarboxylate (PDC)-induced glutamate reuptake blockade on the viability of glial cells in cerebellar granule cell cultures. Immunofluorescence staining for the glial-specific intermediate filament protein, GFAP, revealed that the PDC- induced increase of extracellular glutamate concentration was accompanied by increased astrocyte death, while neurons and oligodendrocytes remained intact and viable. Astrocytic cell death was manifested as fragmentation of processes and cell bodies. The selective astrocyte death was completely prevented by the competitive alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA)/kainate receptor antagonist, NBQX (10 microM), whereas MK-801 (10 microM), a noncompetitive blocker of N-methyl-D-aspartate receptors, gave only partial protection. Double staining for GFAP and the AMPA receptor subunits GluR2/3 showed that astrocytes had much higher immunoreactivity for GluR2/3 than neurons or oligodendrocytes, suggesting that the number of AMPA receptors is likely to be higher on astrocytes. Furthermore, we employed real-time RT-PCR to measure GluR1-4 subunit mRNA expression in control and PDC-exposed cultures. Following treatment with PDC, GluR1 and GluR4 mRNAs were reduced by 40% and GluR3 was reduced by 70% relative to control levels. In contrast, GluR2 expression was not affected by the PDC treatment, indicating that GluR3 was the dominant type of AMPA receptor subunit expressed on astrocytes. Our results show that astrocytes appear to be more vulnerable than neurons or oligodendrocytes to a gradual increase in the extracellular glutamate concentration, suggesting that astrocytes may be critically involved in the pathophysiology of slowly developing chronic neurodegenerative disorders.     

Different dependence of lithium and valproate on PI3K/PKB pathway

Objectives: Acute treatment with valproate (VPA) or lithium (Li⁺) protects cerebellar granule cells (CGC) against apoptosis induced by low potassium (K⁺) (5 mM). As the protection induced by VPA is absolutely dependent on insulin, in contrast to the observed effects of Li⁺, we decided to study the different role of the PI3K/PKB pathway in the neuroprotective effects of both drugs.

Methods: We have studied the neuroprotection elicited by Li⁺ or VPA in cultures of rat CGC. We induced the apoptosis by switching to a medium with a low concentration of K⁺ or by adding C₂-ceramide to the cultures. We studied the effect of Li⁺ and VPA on viability and on the regulation of the PI3K/PKB pathway.

Results and conclusions: Insulin also protects against low K⁺-induced apoptosis in CGC, probably through its interaction with an insulin-like growth factor receptor. Moreover, whereas Li⁺ protects against the apoptosis induced by C₂-ceramide, VPA cannot, probably due to the inhibition of protein kinase B (PKB) caused in this apoptotic stimulus. These results suggest that VPA protects against low K⁺-induced apoptosis by acting on the PI3K/PKB pathway; however, VPA does not affect the increase of PKB activity caused by insulin in these cells. The protection by Li⁺ is independent of this transduction pathway. Moreover, Li⁺ blocks the caspase 3 activation induced by low K⁺, whereas neither VPA nor insulin affects this activation.