复方丹参注射液对动物学习记忆能力的影响

目的:观察并比较复方丹参注射液和吡拉西坦(脑复康)对大鼠和小鼠学习记忆能力的影响。方法:以东莨菪碱和乙醇分别造成动物学习记忆获得障碍和记忆再现障碍,采用迷津法和跳台法进行测试,结果:复方丹参注射液和脑复康对东莨菪碱和乙醇所致的学习记忆障碍均有改善作用(与模型组比较,复方丹参组均为P<0.05,脑复康组均为0.05相似文献   

蝙蝠葛酚性碱对小鼠脑缺血再灌注后软脑膜微循环的影响

目的:观察蝙蝠葛酚性碱对小鼠脑缺血再灌注后软脑膜微循环障碍的改善作用。方法:将60只小鼠随机分为假手术组、缺血再灌注组、蝙蝠葛酚性碱低、中、高剂量组、阳性对照组。用动脉夹夹闭小鼠双侧颈总动脉10 min后去掉动脉夹,制作脑缺血再灌注损伤模型, 应用BI2000微循环图像处理系统,通过开放式颅窗观察各组小鼠软脑膜微静脉、微动脉血流速度和微小血管开放数目,以及蝙蝠葛酚性碱对小鼠脑缺血再灌注后软脑膜微循环障碍的改善作用。结果:缺血损伤组软脑膜微小动脉、静脉血管直径明显缩小,血流速度缓慢,与正常对照组比较,差异有显著意义(P <0.05);蝙蝠葛酚性碱可剂量依赖性增加缺血再灌注所致的软脑膜微小动、静脉血流速度和血管开放数目。结论:蝙蝠葛酚性碱可增加小鼠脑缺血再灌注脑软膜血流量,改善脑缺血后脑软膜微循环障碍,发挥对脑缺血的保护作用。     

蝙蝠葛酚性碱对实验性心肌缺血血流动力学的影响

目的: 观察蝙蝠葛酚性碱对实验性心肌缺血血流动力学的影响.方法: 结扎大鼠左冠状动脉前降支制备急性心肌缺血模型. 结果: 蝙蝠葛酚性碱可显著抑制心肌缺血所致LVEDP的升高和MBP、 dp/dtmax、-dp/dtmax、CO的降低.结论: 蝙蝠葛酚性碱能改善心肌缺血时血流动力学的紊乱,提示蝙蝠葛酚性碱对心肌缺血具有保护作用.     

蝙蝠葛酚性碱对胃癌菏瘤鼠抗肿瘤作用

目的:初步观察蝙蝠葛酚性碱对胃癌小鼠原位移植瘤生长的抑制作用。方法:取50只小鼠建立肿瘤鼠动物模型,测定小鼠瘤重、检测蝙蝠葛酚性碱对肿瘤的抑制率。结果:蝙蝠葛酚性碱各组对荷瘤鼠肿瘤生长具有抑制作用,三个剂量组的抑瘤率分别是55.13%、48.67%、39.92%,与模型对照组比较具有统计学意义(P<0.05)。结论:蝙蝠葛酚性碱对胃癌荷瘤鼠具有抑制作用,本研究为其在临床应用提供了一定的实验和理论依据。     

蝙蝠葛酚性碱在大鼠小肠吸收特性研究

目的研究蝙蝠葛酚性碱在大鼠小肠的吸收特性。方法采用大鼠肠灌流实验,主要从药物吸收部位、浓度和介质pH等三方面对蝙蝠葛酚性碱的吸收特性进行研究。结果蝙蝠葛酚性碱在大鼠小肠吸收速率（Ka）顺序为：回肠＞空肠≈十二指肠;药物浓度对Ka无显著影响;蝙蝠葛酚性碱在pH 5.4,6.8,7.8介质的Ka差异有统计学意义（P＜0.05）。结论蝙蝠葛酚性碱在大鼠小肠各肠段均有一定吸收,但在回肠段吸收更好;蝙蝠葛酚性碱的吸收机制为被动扩散;随着肠循环液pH增大,蝙蝠葛酚性碱Ka增大。     

石菖蒲水提取物SIPI-SCPd改善动物学习记忆的研究

目的研究石菖蒲水提取物SIPI-SCPd是否有改善动物学习记忆的作用。方法将70,35,17.5和8.75 mg/kg的SIPI-SCPd分别连续给予ICR小鼠口服2周或Wistar大鼠口服4周,采用跳台法或避暗法观察其对东莨菪碱、NaNO2及45%乙醇诱导的小鼠记忆损伤(记忆获得障碍,记忆巩固不良,记忆再现障碍)模型的影响,以及采用Morris水迷宫法观察SIPI-SCPd对由东莨菪碱所致大鼠记忆障碍的影响。并观察受试小鼠脑内乙酰胆碱酯酶活力的变化。结果 70,35,17.5 mg/kg的SIPI-SCPd均能延长记忆获得障碍、记忆巩固不良和记忆再现障碍模型小鼠跳下平台或进入暗室的潜伏期;并能改善由东莨菪碱所致的大鼠空间记忆障碍。SIPI-SCPd对乙酰胆碱酯酶的活性没有影响。结论 SIPI-SCPd对几种药物诱导的记忆障碍模型动物的学习记忆功能均有一定的改善作用,且该作用与乙酰胆碱酯酶的活性无关。     

蝙蝠葛酚性碱对BXPC-3肿瘤抑制作甩及外周血IL-1含量的影响

目的观察蝙蝠葛酚性碱对BXPC-3荷瘤裸鼠的肿瘤抑制作用及外周血IL-1含量的影响。方法建立BXPC-3荷瘤裸鼠动物模型,检测蝙蝠葛酚性碱对转移瘤的抑制率;采用ELISA法检测荷瘤小鼠外周血IL-1含量变化。结果蝙蝠葛酚性碱高、中、低剂量对BXPC-3荷瘤裸鼠均有明显抑制肿瘤生长的作用,其抑瘤率分别为34．91％,52．83％和41．51％,可以降低BXPC-3荷瘤小鼠血清IL-1含量。结论蝙蝠葛酚性碱对BXPC-3荷瘤裸鼠具有明显的抑瘤作用,其抑瘤作用可能与降低BXPC-3荷瘤小鼠血清IL-1含量有关,该研究为其临床应用提供了一定的实验和理论依据。     

蝙蝠葛酚性碱对BXPC-3肿瘤抑制作用及外周血IL-1含量的影响

目的观察蝙蝠葛酚性碱对BXPC-3荷瘤裸鼠的肿瘤抑制作用及外周血IL-1含量的影响。方法建立BXPC-3荷瘤裸鼠动物模型,检测蝙蝠葛酚性碱对转移瘤的抑制率;采用ELISA法检测荷瘤小鼠外周血IL-1含量变化。结果蝙蝠葛酚性碱高、中、低剂量对BXPC-3荷瘤裸鼠均有明显抑制肿瘤生长的作用,其抑瘤率分别为34.91%,52.83%和41.51%,可以降低BXPC-3荷瘤小鼠血清IL-1含量。结论蝙蝠葛酚性碱对BXPC-3荷瘤裸鼠具有明显的抑瘤作用,其抑瘤作用可能与降低BXPC-3荷瘤小鼠血清IL-1含量有关,该研究为其临床应用提供了一定的实验和理论依据。     

蝙蝠葛酚性碱对脑缺血再灌注大鼠脑水肿及血脑屏障通透性的影响

目的研究蝙蝠葛酚性碱对脑缺血再灌注大鼠脑水肿及血脑屏障通透性的影响。方法线栓法制备大鼠大脑中动脉阻断局灶性脑缺血模型,缺血2 h后实行再灌注,采用干湿重方法测定脑含水量,用伊文思蓝法(Evans Blue,EB)观察再灌注不同时间点血脑屏障通透性变化,并观察蝙蝠葛酚性碱对不同再灌注时间大鼠脑水肿和血脑屏障通透性的影响。结果蝙蝠葛酚性碱能明显降低脑缺血再灌注大鼠的脑含水量和EB含量。结论蝙蝠葛酚性碱对脑缺血再灌注大鼠脑水肿及血脑屏障通透性具有保护作用。     

蝙蝠葛酚性碱对脑缺血再灌注大鼠脑水肿及血脑屏障通透性的影响

目的 研究蝙蝠葛酚性碱对脑缺血再灌注大鼠脑水肿及血脑屏障通透性的影响.方法 线栓法制备大鼠大脑中动脉阻断局灶性脑缺血模型,缺血2 h后实行再灌注,采用干湿重方法 测定脑含水量,用伊文思蓝法(Evans Blue,EB)观察再灌注不同时间点血脑屏障通透性变化,并观察蝙蝠葛酚性碱对不同再灌注时间大鼠脑水肿和血脑屏障通透性的影响.结果 蝙蝠葛酚性碱能明显降低脑缺血再灌注大鼠的脑含水量和EB含量.结论 蝙蝠葛酚性碱对脑缺血再灌注大鼠脑水肿及血脑屏障通透性具有保护作用.     

Protective effect and its mechanism of codonopsis pilosula polysaccharide on memory consolidation disorder induced by cycloheximide in mice

OBJECTIVE To investigate the protective effect of Codonopsis Pilosula Polysaccharide(CPPS)on improving of the memory consolidation disorder induced by Cycloheximide and its possible mechanisms in mice.METHODS The mice was divided into five groups,as normal control group,cycloheximid model group,piracetam positive control group,CPPS 300 mg·kg~(-1) group,and CPPS150 mg·kg~(-1) group.The mice respectively were given saline,piracetam,and CPPS for 15 d.The memory consolidation disorder model in mice was established by ip.Cyclohexylamine,and orally administered CPPS(300 mg·kg~(-1) or 150 mg·kg~(-1))every day.Then experimental groups were subjected Morris Water Maze test.Western blotting analysis were used to analysis the expression of Ca MKⅡ/CREB signaling pathways.RESULTS Morris water maze experiment showed that cyclohexylamine can cause memory consolidation disorder(P<0.01),and giving piracetam and CPPS(300 mg·kg-1)can improve spatial memory impairment in mice(P<0.05,P<0.01).Western blotting experiment results show that compared with normal control group,Ca MKⅡand CREB contents of brain in model group mice had significant decreased(P<0.001);Compared with model group,Ca MKⅡand CREB contents of brain tissue in piracetam and CPPS groups increased significantly(P<0.05,P<0.01,P<0.001).CONCLUSION Cycloheximide can induce the memory consolidation disorder,and its effect in mice related to Ca MK/CREB signaling pathways.CPPS can improved this memory disorder by influence Ca MKⅡ/CREB signaling pathways.     

Effect of piracetam on urea-induced myoclonus in rats]

Piracetam [2-oxo-1-pyrrolidineacetamide], a cyclic GABA, has been used in Europe for the treatment of patients with cognitive disorders. We investigated the effect of piracetam on urea-induced myoclonus in rats. Myoclonus was induced by intraperitoneal injection of 4.5 g/kg urea, and was recorded with EMG and video apparatus. The incidence of induced myoclonus decreased significantly by intraperitoneal injection of 300 mg/kg piracetam and oral administration of 0.3-10 mg/kg clonazepam. Furthermore, the combined application of 100 mg/kg piracetam and 0.03-0.1 mg/kg clonazepam was effective in ameliorating the myoclonus, although separate administrations were not effective. These findings suggest that piracetam is an effective drug for treating myoclonus, particularly when it is used in combination with clonazepam.     

Reversal of propoxur-induced impairment of step-down passive avoidance, transfer latency and oxidative stress by piracetam and ascorbic acid in rats

Propoxur, a carbamate pesticide has been shown to adversely affect memory and induce oxidative stress. The present study was designed to correlate the effect of propoxur, piracetam (a nootropic drug) and ascorbic acid (an antioxidant) on oxidative stress and cognitive function. Cognitive function was assessed using step-down latency (SDL) on a passive avoidance apparatus and transfer latency (TL) on elevated plus maze. Oxidative stress was assessed by examining brain malondialdehyde (MDA) and non-protein thiol (NP-SH) levels. A significant reduction in SDL and prolongation of TL was found for the propoxur-treated group at weeks 6 and 7 as compared with control (p < 0.001). One week treatment by piracetam (400 mg/kg/d, i.p.) or ascorbic acid (120 mg/kg/d, i.p.) antagonized the effect of propoxur on SDL as well as TL. Both piracetam and ascorbic acid attenuated the propoxur-induced increase in brain MDA levels and decrease in brain NP-SH levels. Results of the present study show that ascorbic acid and piracetam have the potential to reverse cognitive dysfunction and oxidative stress induced by propoxur in the brain.     

Radial maze as a tool for assessing the effect of drugs on the working memory of rats

The effect of physostigmine (0.2 mg/kg), scopolamine (0.1 mg/kg), d,l-amphetamine (1 mg/kg), apomorphine (0.05 mg/kg), and piracetam (100 mg/kg) on working memory was examined in 12 rats that were highly overtrained in the radial maze. In experiment 1, drugs administered 10 min before the trial did not worsen performance of rats in the 12-arm maze. In experiment 2, insertion of a 5-min delay between the sixth and seventh choices increased the number of errors over choices 7–12. Performance was unaffected by pretreatment with physostigmine or apomorphine, but was significantly impaired by scopolamine, amphetamine, and piracetam. In experiment 3, performed in a 24-arm maze, the number of errors and trial duration increased, but performance was not decreased by amphetamine or piracetam. It is concluded that the uninterrupted radial maze task is relatively resistant to pharmacological disruption, but that scopolamine, amphetamine, and piracetam enhance the effect of stimuli interfering with the storage of spatial information over delays.     

The effects of exifone, a new agent for senile memory disorder, on two models of memory in the mouse

The effects of exifone (ADLONE), hexahydro-2,3,4,3',4',5'-benzophenone, were tested in two models of memory in the mouse: habituation of exploratory activity and antagonism of amnesia induced by scopolamine in a passive avoidance task. In the first model, mice which had received exifone (128 and 256 mg/kg IP) 30 minutes before a 3 minute exposure to a staircase exploratory test showed a more marked decrease in exploratory activity in the same apparatus 24 hours later (habituation) than a control group indicating improved memory. Similar results were obtained with piracetam (512 mg/kg, IP). In the second model exifone (512 mg/kg PO), administered 60 minutes before both the learning and retention trials of a standard step-through passive avoidance, task partially antagonized the amnesia induced by 10 mg/kg scopolamine IP administered immediately after the learning trial. Similar results were obtained with piracetam (800 mg/kg PO). Taken together these results suggest that exifone facilitates memory function in simple rodent models in a manner consistent with its supposed therapeutic effects in man.     

Piracetam elevates muscarinic cholinergic receptor density in the frontal cortex of aged but not of young mice

Chronic treatment (2 weeks) with piracetam (500 mg/kg, once daily PO) elevatedm-cholinoceptor density in the frontal cortex of aged (18 months) female mice by about 30–40%, but had no effect onm-cholinoceptor density in the frontal cortex of young (4 weeks) mice. The effect of piracetam onm-cholinoceptor density as determined by the specific binding of tritiated QNB was not affected by concomitant daily treatment with either choline (200 mg/kg) or scopolamine (4 mg/kg). It is concluded that the effect of piracetam onm-cholinoceptor density could explain the positive effects which have been reported for combinations of cholinergic precursor treatment with piracetam on memory and other cognitive functions in aged experimental animals and patients and could also represent part of the possible mechanism of action of piracetam alone.     

Vinpocetine and piracetam exert antinociceptive effect in visceral pain model in mice

The effect of vinpocetine or piracetam on thermal and visceral pain was studied in mice. In the hot plate test, vinpocetine (0.9 and 1.8 mg/kg), but not piracetam, produced a reduction in nociceptive response. Vinpocetine (0.45-1.8 mg/kg, ip) or piracetam (75-300 mg/kg, ip) caused dose-dependent inhibition of the abdominal constrictions evoked by ip injection of acetic acid. The effect of vinpocetine or piracetam was markedly potentiated by co-administration of propranolol, guanethidine, atropine, naloxone, yohimbine or prazosin. The marked potentiation of antinociception occurred upon a co-administration of vinpocetine and baclofen (5 or 10 mg/kg). In contrast, piracetam antagonized antinociception caused by the low (5 mg/kg), but not the high (10 mg/kg) dose of baclofen. The antinociception caused by vinpocetine was reduced by sulpiride; while that of piracetam was enhanced by haloperidol or sulpiride. Either vinpocetine or piracetam enhanced antinociception caused by imipramine. The antinociceptive effects of vinpocetine or piracetam were blocked by prior administration of theophylline. Low doses of either vinpocetine or piracetam reduced immobility time in the Porsolt's forced-swimming test. This study indicates that vinpocetine and piracetam possess visceral antinociceptive properties. This effect depends on activation of adenosine receptors. Piracetam in addition inhibits GABA-mediated antinociception.     

Reversal of propoxur-induced impairment of step-down passive avoidance,transfer latency and oxidative stress by piracetam and ascorbic acid in rats

Propoxur, a carbamate pesticide has been shown to adversely affect memory and induce oxidative stress. The present study was designed to correlate the effect of propoxur, piracetam (a nootropic drug) and ascorbic acid (an antioxidant) on oxidative stress and cognitive function. Cognitive function was assessed using step-down latency (SDL) on a passive avoidance apparatus and transfer latency (TL) on elevated plus maze. Oxidative stress was assessed by examining brain malondialdehyde (MDA) and non-protein thiol (NP-SH) levels. A significant reduction in SDL and prolongation of TL was found for the propoxur-treated group at weeks 6 and 7 as compared with control (p < 0.001). One week treatment by piracetam (400 mg/kg/d, i.p.) or ascorbic acid (120 mg/kg/d, i.p.) antagonized the effect of propoxur on SDL as well as TL. Both piracetam and ascorbic acid attenuated the propoxur-induced increase in brain MDA levels and decrease in brain NP-SH levels. Results of the present study show that ascorbic acid and piracetam have the potential to reverse cognitive dysfunction and oxidative stress induced by propoxur in the brain.     

The differential effects of post-session administration of amineptine and imipramine on memory processes in mice

The effects of post-trial administration of amineptine, a dopaminergic antidepressant drug, were compared with those of memory-facilitating (strychnine, piracetam) or impairing drugs (phenobarbital, imipramine) on an experimental model of memory. Mice were given two sessions in open-field test and the decrease in activity at the second session (habituation) served as an index of retention. The good retention observed with a 1-day inter-session interval was impaired by post-session administration of phenobarbital (10 mg/kg i.p.) or imipramine (5.0 mg/kg i.p.). The poor retention observed with a 5-day inter-session interval was enhanced by post-session administration of strychnine (0.20 mg/kg i.p.), piracetam (1000 mg/kg i.p.) and amineptine (10 mg/kg i.p.). These findings show that different profiles of cognitive and psychomotor effects were produced by imipramine and amineptine. Amineptine, lacking sedative and anticholinergic properties which are characteristic of imipramine, interferes positively with learning and memory, in a manner similar to piracetam and strychnine.