硒锗联合对酒精致大鼠肝脏脂质过氧化的影响

采用体外和体内实验以酒精诱导大鼠肝脏脂质过氧化为模型，研究了（Ｎａ＿２ＳｅＯ＿３）和锗（羧乙基锗倍半氧化物，Ｇｅ－１３２）联合应用的协同抗氧化作用。结果表明，酒精在体外和体内均可导致大鼠肝脏脂质过氧化。体外研究发现将硒和锗同时使用时（Ｎａ＿２ＳｅＯ＿３，２０μｍｏｌ／Ｌ＋Ｇｅ－１３２，１０．５ｍｍｏｌ／Ｌ），表现出比使用相同剂量单一的硒Ｎａ＿２ＳｅＯ＿３，２０μｍｏｌ／Ｌ）或锗（Ｇｅ－１３２，１０．５ｍｍｏｌ／Ｌ）具有更强的抗氧化作用。体内研究将硒和锗剂量减半同时使用（Ｎａ＿２ＳｅＯ＿３，０．０５５ｍｇ／ｋｇ＋Ｇｅ－１３２，１００ｍｇ／ｋｇ），具有类似如单一的较高剂量硒（Ｎａ＿２ＳｅＯ＿３，０．１１ｍｇ／ｋｇ）的抗氧化作用和比使用单一的较高剂量锗（Ｇｅ－１３２，２００ｍｇ／ｋｇ）更强的抗氧化作用。本次研究结果表明硒（Ｎａ＿２ＳｅＯ＿３）和锗（Ｇｅ－１３２）在体外及体内均具有协同抗氧化作用。     

有机锗与环磷酰胺联合应用的研究

通过小鼠骨髓嗜多染红细胞微核实验，观察不同浓度有机锗（Ｇｅ－１３２）与环磷酰胺同时应用时的抗突变效应及其与剂量的关系。实验结果经２×Ｃ表非独立Ｘ２分割的多重比较统计处理，结果显示：在实验条件下，当Ｇｅ－１３２用量大于５０ｍｇ／ｋｇ时，与环磷酰胺有明显的协同作用，并有随Ｇｅ－１３２浓度增加而微核率升高的趋势。只有在适当的浓度（１２．５ｍｇ／ｋｇ），Ｇｅ－１３２才有抗突变作用。提示，Ｇｅ－１３２作为辅助用药在临床化疗或其他治疗时，应注意选择合适的用量范围。     

有机锗与鲨肝醇对苯中毒小鼠升白细胞作用的比较研究

评价有机锗（Ｇｅ－１３２）对苯中毒小鼠白细胞降低的治疗作用在制备动物模型的基础上,将符合诊断标准的动物给予鲨肝醇和不同剂量有机锗治疗。４周后,对其外周白细胞总数、分类、血红蛋白骨髓及脏器系数进行检测。结果显示：Ｇｅ－１３２对人工诱导苯中毒所致的外周白细胞降低有一定的治疗作用,它优于鳖肝醇,以５００ｍｇ／ｋｇ剂量组治疗效果最佳。提示有机锗治疗苯中毒所致的白细胞减少症比鲨肝醇更有效,     

硒和锗拮抗苯致小鼠骨髓细胞微核的实验观察

采用小鼠骨髓嗜多染红细胞微核试验方法观察微量元素硒和锗的抗苯诱变活性。结果：苯吸入染毒（１５ｍｇ／Ｌ×５天，每天２小时）后，小鼠微核率明显增高。在苯处理前３０分钟经口给予不同浓度的亚硒酸钠（００５～２５０ｍｇ／ｋｇ）或锗－１３２（５０～５００ｍｇ／ｋｇ），微核细胞率显著降低，微核抑制率随硒或锗剂量的增加而升高。提示，硒和锗对苯诱导的遗传物质损伤具有保护作用     

有机锗保健作用的评价

有机锗保健作用的评价王兰锗属于稀有元素，在地壳中的平均含量为１．５ｍｇ／ｋｇ，原子量７２．６。２０世纪开始合成有机锗化合物。１９６７年，吉川浩等和浅井一彦合成了有机－β－羧乙基锗倍半氧化物，即Ｇｅ－１３２（ｃａｒｂｏｘｙｅｔｈｙｌｇｅｒｍａｎｉ－ｕｍ...     

Ge—132对高脂血症大鼠脂代谢及肾功能影响的实验研究

在观察Ｇｅ－１３２（羧乙基锗倍半氧化物）对血脂影响的同时，观察了其对肾脏脂质及功能的影响。结果显示：Ｇｅ－１３２３００ｍｇ／ｋｇＷｔ每周２次，能降低血清低密度脂蛋白胆固醇含量，提高高密度脂蛋白胆固醇／总胆固醇比值；Ｇｅ－１３２１００ｍｇ／ｋｇＷｔ，每天１次，对血脂影响不明显，但引起肾脏甘油三酯含量升高，血清尿素氮、血肌酐浓度上升，肌酐清除率下降。     

K-银环蛇毒素对小鼠被动学习和空间记忆的影响

以Ｋ－银环蛇毒素（Ｋ－ＢＧＴ，３．２５μｇ／ｋｇ）海马内注射可造成小鼠胆碱能神经Ｎ受体功能受损的学习记忆的障碍。水迷宫检测结果表明，Ｋ－ＢＧＴ组小鼠空间学习记忆明显下降，训练第４天，逃避潜伏期比第１天下降仅为１６．７％，而对照组逃避潜伏期比第１天下降达５８．３％。在第５天６轮共６０次训练中，对照组在规定时间内找到平台的百分数为８０．０％，而Ｋ－ＢＧＴ组仅为３３．３％。撤去平台后第１天，对照组穿越原平台所在部位的次数为（５．３±２．８）次，而Ｋ－ＢＧＴ仅为（１．９±１．２）次。此外搜寻平台方式构成方面也出现了明显变化。避暗测试结果表明，Ｋ－ＢＧＴ组比对照组潜伏期下降３８．３％，错误率比对照组增加了２．２５倍。卵磷脂４０ｍｇ／ｋｇ经胃灌服１４天对Ｋ－ＢＧＴ所致学习记快损伤具有一定的改善作用，但对正常小鼠学习记忆无明显影响     

Ge—132对人乳癌细胞株BCaP—37的生物学作用

应用细胞培养技术，分子杂交的Ｎｏｒｔｈｅｒｎ Ｂｌｏｔ法和图像细胞分析技术（ＩＣＭ），研究Ｇｅ—１３２对人乳癌细胞株ＢＣａＰ—３７的生物学作用。细胞生长曲线的结果显示，Ｇｅ—１３２的３个实验组（１０．０ｍｇ／Ｌ，１００．０ｍｇ／Ｌ，２００．０ｍｇ／Ｌ）对细胞的生长没有显著抑制作用，并对细胞的毒性作用很小。基因检测显示，高浓度Ｇｅ—１３２（２００．０ｍｇ／Ｌ）对癌基因Ｃ—ｅｒｂＢ，和癌相关基因ＥＧＦＲ ｍＲＮＡ的表达具有抑制作用。ＩＣＭ的四项指标显示，Ｂ和Ｃ两实验组（１０．０ｍｇ／Ｌ，２００．０ｍｇ／Ｌ）ＤＩ值呈异倍体。表现为恶性细胞的特征，两组核面积显著低于对照组（Ｐ＜０．０ｌ）：Ｃ组的Ｓ期百分比显著低于对照组（Ｐ＜０．０５）。综合评价ＩＣＭ各项指标发现，Ｇｅ—１３２（２００．０ｍｇ／Ｌ）对细胞的增殖有一定抑制作用。     

Ge－132治疗骨质疏松症的实验结果

Ｇｅ－１３２为一种有机锗化合物，本文回顾了它对治疗老年性骨质疏松症的效果。８名患该病的妇女，服Ｇｅ－１３２１年，服后３个月，桡骨骨盐含量显著大于对照组（Ｐ＜０．０５），血清ＡＬＰ、ＰＴＨ皆显示有意义的减少。大鼠切除卵巢导致骨质疏松模型，给以Ｇｅ－１３２，能提高股骨横向强度及骨密度，改善血清降钙素及ＰＴＨ含量，说明Ｇｅ－１３２能避免骨质疏松造成的骨量减少。给小猎犬静脉注射Ｇｅ－１３２（５００ｍｇ／Ｋｇ）６个月，未看到血清Ｃａ、Ｐ代谢异常及肾功能ＢｕＮ生化指标变化。     

尼古丁对小鼠海马结构c—fos蛋白表达的影响

为了研究尼古丁对学习记忆的影响，我们利用免疫组织化学技术，研究尼古丁对跳台学习小鼠海马结构ｃ－ｆｏｓ蛋白表达的影响。结果显示，虽然５分钟的小鼠跳台学习成绩（错误数）实验组与对照组相比，差异没有显著性，但给药２小时后海马结构ｃ－ｆｏｓ蛋白表达有所不同，其中２ｍｇ／ｋｇ尼古丁剂量组在海马ＣＡ３区和齿状回部位的ｃ－ｆｏｓ阳性细胞数比１ｍｇ／ｋｇ尼古丁剂量组及对照生理盐水组显著增多（Ｐ＜０．０１），而１ｍｇ／ｋｇ尼古丁剂量组与对照生理盐水组差异无显著性。提示２ｍｇ／ｋｇ尼古丁剂量可能对学习记忆有损害作用。     

锂对染铅大鼠海马胆囊收缩素和神经元型一氧化氮合酶神经元的保护作用

目的 探讨锂对染铅大鼠海马胆囊收缩素（CCK）和神经元型一氧化氮合酶（nNOS）神经元的保护作用及其与动物学习记忆功能变化的关系.方法 通过测量体重,利用反映学习记忆功能的Y迷宫法和ABC免疫组化法,研究饮用含0.2 g/L醋酸铅（PbAc）水和含不同剂量（3、30、300、3 000mg/kg）氯化锂（LiCl）饲料喂养的大鼠体格发育情况、学习记忆能力以及海马不同亚区CCK和nNOS阳性神经元数目的变化.结果铅染毒组大鼠体重增加少于对照组大鼠,差异有统计学意义（P＜0.05）,Y-迷宫学会次数多于对照组大鼠,差异有统计学意义（P＜0.05）;其海马各区CCK和nNOS阳性神经元数明显减少,差异有统计学意义（P＜0.05）.铅＋LiCl（3、30、300mg/kg）组体重增加多于对照组大鼠,差异有统计学意义（P＜0.05）;Y-迷宫学会次数少于对照组大鼠,差异有统计学意义（P＜0.05）,海马各区CCK阳性神经元数明显增加,差异有统计学意义（P＜0.05）.铅＋3 000mg/kg LiCl组大鼠Y-迷宫学会次数多于对照组大鼠,差异有统计学意义（P＜0.05）;海马各区CCK阳性神经元数明显少于对照组,差异有统计学意义（P＜0.01）;与铅染毒组比较,差异无统计学意义（P＞0.05）.结论 铅可损伤大鼠学习记忆能力,影响大脑海马CCK和nNOS阳性神经元的数目.较低剂量的锂对铅引起的学习记忆损伤和海马CCK阳性神经元的变化有一定保护作用.     

硫酸锌和牛磺酸锌对铅染毒大鼠体重及学习记忆的影响

目的　探讨硫酸锌 (ZnSO4)和牛磺酸锌 (TZC)拮抗铅损害神经系统的作用。方法　采用测量体重增量和Y型迷宫实验 ,观察饮用 0 2 g/L 醋酸铅水溶液和含不同剂量ZnSO4(5 ,15 g/kg)、TZC(5 9,17 7g/kg) 饲料喂养的大鼠与饮用单蒸水和普通饲料喂养的大鼠之间体重增量和学习记忆能力的差别。结果　与对照组相比 ,铅染毒大鼠体重增量明显减少 (P <0 0 5 ) ,完成Y -迷宫实验次数明显增多(P <0 0 5 ) ;补充不同剂量ZnSO4和TZC对铅染毒大鼠体重增量和学习记忆均有明显改善作用 ,其中以低剂量TZC和高剂量ZnSO4效果更好。结论　锌能明显促进铅染毒大鼠体重增加及学习记忆能力增强。锌对铅损害神经系统有明显的拮抗作用。     

Postnatal lead exposure alters spontaneous cerebellar Purkinje neuron discharge

The effects of early postnatal lead administration on the spontaneous activity of cerebellar Purkinje neurons were studied electrophysiologically in adult male Sprague-Dawley rats. Newborn rat litters were divided into three groups and injected daily from Day 1 to Day 20 after birth with 8 mg NaAc/kg, 1 mg PbAc/kg, or 8 mg PbAc/kg intraperitoneally. Purkinje neurons in all three groups showed regular and sustained discharge. However, the mean spontaneous firing rate was significantly lower in the 8-mg PbAc/kg group (26.13 ± 1.28 Hz) compared to the NaAc controls (32.39 ± 1.93, P > 0.01). Furthermore, the distribution of the firing rates of the Purkinje cells were different in the two groups, with an obvious loss of faster firing cells in the 8-mg PbAc/kg group. No differences were seen between the 1-mg PbAc/kg group and the NaAc controls. As the 8-mg PbAc/kg group weighed significantly less than the NaAc group, malnourished animals were produced by using oversized litters, to control for any changes caused by the lower body weight. However, when compared to concomitantly raised controls, no changes could be seen in Purkinje cell discharge in the malnourished animals. It is concluded that neonatal exposure to lead can cause permanent changes in spontaneous Purkinje cell discharge.     

Memory-strengthening activity of Glycyrrhiza glabra in exteroceptive and interoceptive behavioral models

In the traditional system of medicine, the roots and rhizomes of Glycyrrhiza glabra have been employed clinically for centuries for their anti-inflammatory, anti-ulcer, expectorant, antimicrobial, and anxiolytic activities. The present study was undertaken to investigate the effects of G. glabra, popularly known as liquorice (Mulathi), on learning and memory. The elevated plus-maze and passive avoidance paradigm were employed to evaluate learning and memory parameters. Three doses (75, 150, and 300 mg/kg p.o.) of aqueous extract of G. glabra were administered for 7 successive days in separate groups of mice. The dose of 150 mg/kg of the aqueous extract of liquorice significantly improved learning and memory of mice. Furthermore, this dose reversed the amnesia induced by diazepam (1 mg/kg i.p.), scopolamine (0.4 mg/kg i.p.), and ethanol (1 g/kg i.p.). Anti-inflammatory and antioxidant properties of liquorice may be contributing favorably to the memory enhancement effect. Since scopolamine-induced amnesia was reversed by liquorice, it is possible that the beneficial effect on learning and memory may be because of facilitation of cholinergic transmission in brain. However, further studies are necessitated to identify the exact mechanism of action. In the present investigation, G. glabra has shown promise as a memory enhancer in both exteroceptive and interoceptive behavioral models of memory.     

Improvement of mouse memory by Myristica fragrans seeds

Memory is one of the most complex functions of the brain and involves multiple neural pathways and neurotransmitter systems. The present study was undertaken to investigate the effect of Myristica fragrans (MF) seeds on learning and memory in mice. The n-hexane extract of MF was administered orally in three doses (5, 10, and 20 mg/kg p.o.) for 3 successive days to different groups of young and aged mice. The learning and memory parameters were assessed using elevated plus-maze and passive-avoidance apparatus. The effect of MF extract on scopolamine (0.4 mg/kg i.p.)- and diazepam (1 mg/kg i.p.)-induced impairment in learning and memory was also studied. MF extract at the lowest dose of 5 mg/kg p.o. administered for 3 successive days significantly improved learning and memory of young and aged mice. This extract also reversed scopolamine- and diazepam-induced impairment in learning and memory of young mice. MF extract enhanced learning and retention capacities of both young and aged mice. The exact mechanism of the memory-improving effect of MF extract was not explored in the present study. But, the observed memory-enhancing effect may be attributed to a variety of properties (individually or in combination) the plant is reported to possess, such as antioxidant, anti-inflammatory, or perhaps procholinergic activity.     

单唾液酸神经节苷脂对铅暴露大鼠海马神经细胞生长抑素表达的干预作用

目的 研究单唾液酸神经节苷脂（GM1）对铅暴露大鼠海马神经细胞生长抑素（SS）的影响。方法 成年SD大鼠60只，随机分为三组：对照组、染铅组及GM1干预组，20只／组，40只染铅动物饮用0．1％的醋酸铅去离子水三个月，制成慢性染铅大鼠模型。GM1干预组腹腔注射GM1 50mg／kg，对照组和染铅组腹腔注射等量生理盐水，连续14d。采用免疫组化的方法测定大鼠海马细胞SS，观察铅暴露及GM1对其阳性表达的影响。结果 染铅组大鼠学习记忆能力较对照组明显减低，海马CA1区SS阳性神经元数量减少，差异有统计学意义（P〈0．05）；腹腔注射神经节苷脂后，Y-迷宫错误次数减少，其海马CA1区SS阳性神经元数量增多，差异有统计学意义（P〈0．05），CA1区SS阳性神经元数量亦增多但差异无统计学意义（P〉0．05）。结论 外源性神经节苷脂有可能增强海马细胞SS的阳性表达．从而一定程度的改善染铅大鼠的肇习记忆能力。