壳聚糖磷脂复合物治疗痴呆模型鼠的实验研究

目的观察壳聚糖磷脂复合物对痴呆模型大鼠的治疗效果,初步探讨其作用机制.方法将50只SD大鼠随机分为5组(每组10只),分别为:空白对照组(1组)、假手术组(2组)、痴呆模型组(3组)、脑复康治疗组(4组)和壳聚糖磷脂复合物治疗组(5组).分别观察各组大鼠Morris水迷宫逃逸潜伏期、脑电超慢涨落图S谱线、投射电镜下脑组织的超微结构及免疫组织化学及图像分析检测脑组织乙酰胆碱酯酶和基底神经生长因子含量.所得资料应用SAS 6.12进行统计学处理.结果壳聚糖磷脂复合物可以缩短痴呆鼠逃逸时间,提高S5谱线频率,与痴呆模型组(P<0.01)和脑复康治疗组(P<0.05)相比均有统计学意义;可以恢复提高大脑皮层和基底核胆碱能神经元的数量、面积和光密度(P<0.01),减少损伤脑组织变性水肿;脑复康治疗组和壳聚糖磷脂复合物治疗组脑内神经生长因子含量较痴呆模型组有所提高,但无统计学差异(P>0.05).结论壳聚糖磷脂复合物能改善痴呆大鼠的学习和记忆功能,可能与阻止和修复胆碱能神经元损伤,增加乙酰胆碱含量,以及参与脑组织抗炎免疫反应有关.     

苦碟子注射液联合吡拉西坦治疗急性脑梗死的临床研究

目的 探讨苦碟子注射液联合吡拉西坦治疗急性脑梗死的临床疗效。方法 选取2021年7月—2022年7月在开封市人民医院治疗的114例急性脑梗死患者,随机分为对照组（57例）和治疗组（57例）。对照组患者静脉滴注注射用吡拉西坦,4 g加入生理盐水250 mL,1次/d。治疗组在对照组基础上静脉滴注苦碟子注射液,40 mL加入生理盐水250 mL,1次/d。两组患者连续治疗14 d。观察两组患者临床疗效,比较治疗前后两组患者美国国立卫生研究院卒中量表（NIHSS）、脑卒中专门化生活质量表（SS-QOL）和Barthel指数评分,梗死灶体积及脂蛋白相关磷脂酶A2(Lp-PLA2)、S100蛋白（S100β）、泛素羧基末端水解酶-L1(UCH-L1)、谷胱甘肽过氧化物酶（GSH-Px）、超氧化物歧化酶（SOD）和中性粒细胞/淋巴细胞比值（NLR）水平。结果 治疗后,对照组临床有效率为85.96%,治疗组临床有效率为96.49%,两组比较差异具有统计学意义（P<0.05）。治疗后,两组NIHSS评分较治疗前明显下降,而SS-QOL、Barthel指数评分明显升高（P<0.05）,且治疗...     

Effects of four non-cholinergic cognitive enhancers in comparison with tacrine and galanthamine on scopolamine-induced amnesia in rats

Amnesia can be induced in rats in the passive avoidance paradigm by administration of scopolamine, a central muscarinic receptor antagonist. Tacrine or galanthamine, inhibitors of acetylcholinesterase, given in conjunction with scopolamine partially reversed the scopolamine-induced deficit in passive avoidance performance. Four so-called cognitive enhancers, all widely used for the treatment of the symptoms associated with mental aging, cerebral insufficiency and senile memory disorder, were investigated in this paradigm. Piracetam, an extract of Ginkgo biloba, dihydroergocristine and a combination of raubasine with dihydroergocristine, all attenuated the amnesia induced by scopolamine. In contrast, nicergoline had no significant effect. Raubasine alone also failed to significantly attenuate scopolamine-induced amnesia, although some doses of raubasine had a non-significant tendency (P<0.10) to reduce the amnesia.     

Effects of piracetam alone and in combination with antiepileptic drugs in rodent seizure models

Summary. The nootropic drug piracetam was investigated in various experimental models of epilepsy. Generally, piracetam exhibits no or only moderate anticonvulsant properties against generalized tonic or clonic seizures. However, in many cases it did increase the anticonvulsant effectiveness of conventional antiepileptics, as shown in the maximal electroshock seizure (MES) threshold test, the traditional MES test or in DBA/2 mice. A pharmacokinetic interaction does not seem to be responsible for this effect. In lethargic mice, a model of absence seizures, piracetam significantly decreased the incidence and duration of spike-wave discharges. Furthermore, in the cobalt-induced focal epilepsy model piracetam reduced the number of spikes/min and in the hippocampal stimulation model it increased the anticonvulsant potency of phenobarbital and phenytoin after single and repeated administration. In conclusion, the well tolerated piracetam itself did not show marked anticonvulsant effects in most screening tests, however, its co-medication with antiepileptic drugs improved seizure protection in various models which may bear potential clinical significance.     

DOES PIRACETAM COUNTERACT THE ECT-INDUCED MEMORY DYSFUNCTIONS IN DEPRESSED PATIENTS?

A double-blind, intra-individual cross-over comparison of the effect of piracetam on retrograde memory impairment as measured by the KS memory test battery was performed in connection with second and third Bi-ECT in 18 inpatients diagnosed as suffering from depression. The seizure duration and the post-ECT EEG patterns were examined visually and the post-ECT confusion time was measured. Piracetam was given orally in the dose of 4.8 g/day for 3 days. No significant effects were obtained on memory scores, electrical stimulus duration, EEG pattern or post-ECT confusion time. The findings may indicate that the protective effect of piracetam shown in animal electroconvulsive stimulation (ECS) is due to a counteraction of the disturbing effect of hypoxia on memory functions. It is concluded that more information is needed as regards the pharmacokinetics and the mode of action of the drug.     

Effects of piracetam (SKF 38462) on acquisition,retention, and activity in the goldfish

Goldfish treated by immersion with the drug piracetam (SKF 38462 or UCB 6215) in their home tanks obtained higher mean levels of correct active dark-avoidance responding than non-drug-treated controls; the difference did not emerge until the last two days of the five days of training. In another experiment, fish immersed in the drug solution before a single session of group training for dark avoidance scored more correct responses during retention testing than fish exposed to only water before training. However, no difference in correct retention responding was found between fish exposed, during the interval between training and testing, to the drug solution and fish exposed to only water. General activity during retention testing was unaffected with respect to pretraining immersion in water or drug solution; however, immersion in the drug solution between training and testing resulted in lower levels of general activity during retention testing.This work was supported in part by the Tennessee Department of Mental Health; by a General Research Support Fellowship from the University of Tennessee College of Medicine (to RCB); and by a National Institutes of Health Fellowship No. 1 FO2 GM51238-01-NIGMS (to FP).     

The 2-oxopyrrolidinacetamide piracetam reduces infarct brain volume induced by permanent middle cerebral artery occlusion in male rats

In this study, the temporal development of focal cerebral infarction induced by permanent middle cerebral artery occlusion (pMCAO) and the effects of piracetam, a derivative of gamma-aminobutyric acid widely used in clinical practice as a nootropic agent, on infarct area and volume were investigated. pMCAO caused a cerebral infarct whose size progressively increased after 3, 6, 9, and 24 h. Piracetam (125 mg/kg i.p.), administered 6, 9, and 22 h after pMCAO, did not reduce pMCAO-induced brain infarct area size detected at the 24th hour. By contrast, when this agent was administered at the doses of 250 and 500 mg/kg, it caused a marked reduction of the infarct area size. This reduction was observed in almost every brain slice affected by pMCAO, although statistical differences (p <0.05) were detected in slices located at 3-5.5 mm posterior to the anterior pole in animals treated with 250 mg/kg piracetam and in slices located at 3.5-5 mm in those receiving 500 mg/kg. When the mean total volumes of brain infarct resulting from pMCAO were calculated, it was observed that in animals which had received piracetam (250 or 500 mg/kg) infarction volume was markedly ( approximately 50%) and significantly (p <0.05) reduced in comparison with saline injected rats. Finally, piracetam (250 mg/kg administered i.p. 6, 9, and 22 h after the ischemic insult) significantly reduced brain infarct area evaluated 48 h and 7 days after pMCAO.     

Analysis of two mixtures containing racetams in their pharmaceuticals using simple spectrophotometric methodologies

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Antiamnesic activity of Syzygium cumini against scopolamine induced spatial memory impairments in rats

We evaluated the Antiamnesic effects of methanolic extract of Syzygium cumini (MESC) on spatial memory impairments induced by scopolamine (1 mg/kg, i.p.), a muscarinic antagonist, using the Radial arm maze, Morris water maze, learned helpless ness tests. Effect of MESC was evaluated and compared to standard drug, piracetam (200 mg/kg, i.p.). The MESC significantly (p < 0.05) improved the impairment of short term or working memory induced by scopolamine in the Radial arm maze test, and significantly (p < 0.05) reversed cognitive impairments in rats as measured by the learned helplessness test. In addition, MESC decreased escape latencies in the Morris water maze test. The activity of acetylcholinesterase in the brain was inhibited significantly (p < 0.05) by treatment with MESC to a level similar to that observed in rats treated with piracetam. Moreover treatment with MESC (200 and 400 mg/kg, p.o.) to scopolamine induced rats significantly (p < 0.05) decreased TBARS levels which was accompanied by an increase in the activities of SOD and Catalase. MESC has dose dependent effect and 400 mg/kg dose shown more prominent results when compared to 200 mg/kg dose of MESC. These results indicate that MESC may exert anti-amnesic activity via inhibition of acetylcholinesterase and antioxidant mechanisms in the brain.     

吡拉西坦注射液联合甘露醇治疗脑出血脑水肿的临床研究

目的观察吡拉西坦注射液联合甘露醇治疗脑出血脑水肿的临床效果及安全性。方法将我院近1年多来收治的65例脑出血患者,随机分为治疗组和对照组,出血量在15～40ml之间,两组的基础治疗用药神经保护剂相同,治疗组33例应用20%吡拉西坦注射液100ml静脉滴注,2次/天,连续应用10天,同时应用20%甘露醇125ml静脉滴注,q12h/q8h;对照组32例,应用20%甘露醇125ml静脉滴注,q8h/q6h,连续应用10天;每天观察患者用药后头痛、视乳头水肿及意识状况的改变,采用全国第4届脑血管病会议神经功能缺损程度(SSS)评分判定临床疗效。同时检测用药前及用药后24h的尿量及尿比重变化。在用药后15天时复查颅脑CT观察血肿的体积以及血肿周围脑水肿的变化。结果两组患者主要临床症状如头痛、呕吐、视乳头状态及意识障碍等较给药前均有改善,治疗后15天时治疗组症状显效率为67%(22/33),对照组为56%(18/32),两组间有显著性统计学差异(P=0.038);治疗组用药后24h平均尿量为(3644.5±210.4)m1,对照组患者用药后24h的尿量为(3341.9±205.3)ml,两组间具有显著性统计学差异(P<0.05);治疗组用药后平均尿比重为(1.013±0.027),对照组用药后平均尿比重为(1.019±0.030),两组间无显著性统计学差异。治疗15天时CT显示治疗组血肿体积减少(9.9±3.3)ml,水肿平均缩小面积(18.3±2.3)cm2,对照组血肿体积减少(8.0±2.8)ml,水肿平均缩小面积(15.1±2.0)cm2,两组间有显著性统计学差异(P<0.05)。治疗组患者未出现血尿、失眠、兴奋及脏器功能损害等情况。结论吡拉西坦注射液联合甘露醇治疗脑出血继发的脑水肿优于单纯应用甘露醇,并且安全性好。