抗抑郁候选化合物GL-21对大鼠脑皮质中神经递质含量影响的研究

目的:研究抗抑郁候选化合物GL-21对大鼠脑皮质中神经递质去甲肾上腺素(NE)及5-羟色胺(5-HT)含量的影响。方法:采用微透析法取样和高效液相色谱法测定大鼠脑皮质中NE及5-HT的含量。结果:分别给大鼠GL-21 2,4和8 mg/kg后,可大幅增加大鼠脑皮质中神经递质NE及5-HT的含量(P<0.05 or P<0.01),且呈一定的剂量关系。结论:抗抑郁候选化合物GL-21可增加大脑皮质单胺类递质NE及5-HT含量。     

七十味珍珠丸对脑损伤大鼠脑内单胺类神经递质的影响

通过对脑损伤大鼠脑内单胺类神经递质含量的测定,研究七十味珍珠丸治疗脑血管疾病的作用机理.ig给药后,制成脑损伤病理模型,采用荧光分光光度法检测脑内5-羟色胺(5-HT)、去甲肾上腺素(NA)、多巴胺(DA)含量.结果七十味珍珠丸显著降低脑损伤所致大鼠脑内5-HT,NA含量升高,对DA含量的抑制,也有一定作用趋势.     

七十味珍珠丸对脑损伤大鼠脑内单胺类神经递质的影响

目的 :通过对脑损伤大鼠脑内单胺类神经递质含量的测定 ,研究七十味珍珠丸 (RNSP)治疗脑血管疾病的作用机理。方法 :RNSP ig给药后 ,制成脑损伤病理模型 ,采用荧光分光光度法检测脑内 5 -羟色胺 (5 -HT)、去甲肾上腺素 (NA)、多巴胺(DA)含量。结果 :RNSP具有显著降低脑损伤所致大鼠脑内 5 -HT、NA含量升高的作用 (P<0 .0 5、P<0 .0 1) ,对 DA含量的抑制 ,也有一定的作用趋势 (P>0 .0 5 )。结论 :RNSP治疗脑血管疾病的作用机理 ,可能与它具有调节脑内单胺类神经递质的作用有关     

半夏泻心汤对偏头痛大鼠神经递质及早快基因表达的影响

目的 研究半夏泻心汤(BXXXT)对实验性偏头痛模型大鼠神经递质及早快基因表达的影响.方法 将60只SD健康大鼠随机分为正常组、模型组、阳性组、BXXXT高、中、低剂量组.ig生理盐水予正常组、模型组大鼠,其余各组大鼠ig BXXXT,连续7d,末次给药后1h皮下注射硝酸甘油10 mg·kg-1造模.用ELISA法测定大鼠血清中5-羟色胺(5-HT)、5-羟吲哚乙酸(5-HIAA)、多巴胺(DA)、去甲肾上腺素(NE)的含量;HE染色观察大鼠脑干组织细胞形态学的变化;免疫组化染色测定大鼠脑干中c-jun基因的表达.结果 与模型组比较,BXXXT可升高大鼠血浆中DA、NE、5-HT的水平,降低5-HIAA水平和大鼠脑干中c-jun基因的表达.结论 BXXXT对实验性偏头痛大鼠具治疗作用.     

单胺类神经递质在药物成瘾中的作用机制

药物成瘾是一种慢性复发性大脑疾病,各种成瘾性药物通过作用于奖赏系统,最终引起神经递质释放的改变,产生奖赏效应。其中,单胺类神经递质5-羟色胺(5-hydroxytryptamine,5-HT)、去甲肾上腺素(noradrenergic,NE)和多巴胺(dopamine,DA)在药物成瘾中起到重要作用,该文就单胺类神经递质在药物成瘾中的作用及机制进行综述。     

毛细管电泳法分离分析去甲肾上腺素等单胺类神经递质及肾上腺素

利用毛细管电泳法分离去甲肾上腺素 ,5 -羟色胺以及多巴胺三种单胺类神经递质以及肾上腺素。采用自由区带电泳法 ,4 0mmol/L硼砂缓冲液 2 0PSI气压进样 5s,定电压 2 0KV分离 12min。结果显示四种物质完全分离     

都可喜对慢性间断性缺氧大鼠学习记忆能力及脑内单胺类神经递质的影响

目的:探讨都可喜(Duxil,阿米三嗪+萝巴新)对慢性间断性缺氧(EHYP)大鼠学习记忆能力和脑内单胺类神经递质水平的影响。方法:建立EHYP大鼠模型,并给予Duxil(0.03片·350g~(-1)体重,bid)干预。用被动避暗回避反射试验评价大鼠学习记忆能力,潜伏期(STL)越长,学习记忆能力越强;用高效液相色谱电化学检测器法测定大鼠皮层、海马和纹状体内去甲肾上腺素(NE)、多巴胺(DA)和5-羟色胺(5-HT)等单胺类神经递质的含量。结果:与对照组相比,EHYP组大鼠STL明显缩短(P<0.01),各脑区单胺类神经递质水平显著降低(P<0.05)。与EHYP组相比,Duxil组大鼠STL显著延长(P<0.01),皮层NE和DA含量、海马NE,DA和5-HT含量以及纹状体NE,DA和5-HT含量显著升高(P<0.05)。结论:Duxil可改善EHYP大鼠学习记忆能力并提高脑内单胺类神经递质水平。     

前胡提取物对抑郁症模型大鼠脑内中枢单胺类神经递质的影响研究

目的：研究前胡提取物中香豆素类化合物对抑郁症模型大鼠脑内中枢单胺类神经递质的影响。方法以孤养加慢性轻度不可预见性应激方法建立大鼠抑郁症模型,测定糖水消耗、敞箱行为及跳台行为来进行行为学评分,并采用高效液相－电化学方法检测其脑内单胺类神经递质的含量,观察模型大鼠给药前后的变化。结果抑郁症模型组大鼠体质量增长缓慢,蔗糖水消耗量明显下降,水平活动和垂直活动均显著下降,跳台错误次数增加,脑内的去甲肾上腺素、5－羟色胺含量降低（P＜0．05）。30mg／（kg? d）、50mg／（kg? d）剂量前胡提取物能显著改善模型大鼠的行为学变化,增加其脑内去甲肾上腺素、5－羟色胺含量（ P＜0．05）。结论前胡提取物中香豆素类化合物具有抗抑郁作用,对中枢单胺类神经递质的调节作用是其作用机制之一。     

镍对小鼠脑组织ATP酶、钙调素的影响

镍化合物是一类多器官毒物 ,可累及肝、肾、肺、心血管和血液等多种组织器官 ,并具有致癌、致畸、致突变作用[1,2 ] 。据报道可溶性镍盐动物急性毒性可致震颤、舞蹈症、瘫痪等神经系统症状及中枢神经系统水肿[3 ] 。近年来的研究发现 :某些二价金属离子的毒效应与细胞内钙稳态失调有关[4] 。但镍化合物的中枢神经系统毒性的研究 ,国内外少见报道。因此 ,我们采用膜毒理学方法检测脑突触体膜ＡＴＰａｓｅ活力及钙调素(ＣａＭ)含量 ,以探讨镍致神经系统损伤的机制。1　材料与方法1 1　实验动物与分组　健康昆明种小鼠 4 0只 ,雌雄各半 ,体重 1…     

硫酸镍对大鼠生殖细胞的影响

镍（Ni）是人体必需的微量元素，也是环境污染物之一，过量的Ni摄入可造成机体多系统，多器官损伤。研究发现，Ni可透过血睾屏障，对雄性动物的生殖功能造成不良影响。本研究旨在通过应用流式细胞术来进一步探讨硫酸镍（NiSO4）对雄性大鼠睾丸损伤的细胞类型及其细胞周期的变化。     

川续断对D—半乳糖所致衰老模型小鼠抗氧化系统影响的实验研究

本实验采用D－半乳糖衰老模型小鼠,通过测定其红细胞超氧化物歧化酶（SOD）,肝细胞膜Na^ ,K^ -ATPase活性,肝组织丙二醛（MDA）含量,观察上述指标的随龄变化并了解自由基对机体的损伤程度以及川续断在不同用药时间（15、30、45d）对老龄小鼠上述指标的影响,实验结果显示,D－关乳糖可诱导小鼠产生拟衰老改变,川续断可提高老龄小鼠红细胞SOD和肝细胞膜Na^ ,K^ -ATPase活性（P＜0.01）,降低肝组织MDA含量（P＜0.01）。结果提示,川续断具有一定的抗氧化作用。     

硫酸镍诱导大鼠睾丸细胞凋亡的研究

镍(Ni)既是人体的必需微量元素，参与人体的许多正常代谢过程，又是常见的环境污染物之一。属于一种多器官、多系统毒物，并且对生殖系统具有一定的损伤，但其详细机制不清。本研究拟通过雄性动物整体染毒硫酸镍(NiSO4)，探讨Ni对男性生殖系统睾丸的损伤及其机制，为Ni毒性的防治提供实验室理论依据。     

Ginseng saponins: influence on neurotransmitter uptake in rat brain synaptosomes.

The total ginsenoside ( N-butanol extract) fraction inhibited the uptake of radioactive gamma-aminobutyrate (GABA), glutamate (Glu), dopamine (DA), noradrenaline (NA), serotonin (5-HT), but not the uptake of 2-deoxy- D-glucose (2-DG) and leucine (Leu) into rat brain Synaptosomes. Among the ginsenoside fractions investigated, Fraction III which contains mainly R (d) was most effective in reducing the uptake of neurotransmitters. The inhibition was in the order of GABA = NA > DA > Glu > 5-HT, and this effect was concentration-dependent. This inhibitory effect appears to be specific as this fraction, at several concentrations, failed to influence the uptake of 2-DG and Leu significantly. Similar studies indicated that ginsenoside R (c) could affect neurotransmitter uptake specifically as well. Since the GABA uptake was most sensitive to the inhibitory action of these ginsenosides, it is postulated that ginseng may exert its action(s) in the central nervous system by affecting the removal of neurotransmitter substances in synaptic regions and that the GABA-nergic neurons may be one of the major sites of action.     

微动引起人工关节无菌性松动的实验研究

目的　研究一定参数的微动对骨组织生长分化的影响。方法　用特制的骨微动室模型 ,通过动物实验分别计算在无微动组 (A组 )、微动组 (B组 )、微动后停止微动组 (C组 )长入骨微动室模型中的骨组织占所有新生组织的比例。结果　在A组及C组中可见大量不成熟新生骨形成 ,B组可见少量或无新生骨组织可见 ,但可见大量的纤维结缔组织。A组中 ,骨组织占新生组织的比例为 4 0 65 %± 8 2 5 % ,B组为 6 65 %± 2 3 4 % ,C组为 3 5 5 5 %± 6 96%。结论　一定参数的微动可以显著抑制骨组织的形成而有利于纤维组织的形成。当微动停止后 ,原有的纤维组织又可重新由骨组织替代。     

薄层扫描法测定小鼠脑内4种神经递质的含量

用双波长薄层扫描法测定小白鼠脑内的 γ-氨基丁酸、丙氨酸、谷氨酸和牛磺酸四种神经递质的含量 ,测定波长为 λS=50 0 nm,λR=70 0 nm,展开剂为苯酚 -甲酸 -水 (18∶ 2∶ 1) ,显色剂为 1%茚三酮乙醇液 ;75℃～ 80℃烘干 ,结果斑点分离清晰 ,Rf 值适中。四种成分的回收率分别为 10 0 .7% (γ-氨基丁酸 ) ,10 1.1% (丙氨酸 ) ,10 0 .5% (谷氨酸 ) ,10 0 .4 % (牛磺酸 )。     

Morphine and neurotransmitter substances: Microiontophoretic study in the rat brain stem

1 The effects of microiontophoretically applied morphine and its interactions with the effects of microiontophoretic applications of either acetylcholine, (-)-noradrenaline or 5-hydroxytryptamine have been studied on single neurones in the brain stem of rats anaesthetized with urethane.2 Morphine excited or inhibited most neurones tested and the effects, especially excitation, were often extremely powerful. However, the time course of the excitatory and inhibitory effects were somewhat different.3 Desensitization to the excitation produced by morphine was seen after repeated or prolonged applications and it is suggested that this phenomenon may be related to the tolerance which develops after chronic administration of morphine. No desensitization was observed to inhibition of neuronal activity by morphine.4 Morphine usually reduced the excitation of neurones by acetylcholine, noradrenaline or 5-hydroxytryptamine but sometimes potentiated the effect, although not always on the same neurones. Inhibition of neuronal activity by these compounds was never modified by morphine and neither were the effects of glutamate or D,L-homocysteic acid when used as control agonists.5 The in vitro release of morphine from six micropipettes was determined and the transport number was calculated to be 0.051 (s.d. 0.021).6 The implications of these observations in explaining the pharmacological actions of morphine are discussed.     

硫酸壳聚糖体内抗肿瘤作用的实验研究

目的：研究硫酸壳聚糖的体内抗肿瘤作用。方法：用高、低（200、100mg/kg）两个剂量的硫酸壳聚糖分别腹腔注射治疗肉瘤180（S180）小鼠和艾氏腹水癌（EAC）小鼠10d,然后测定其抑瘤率、重要器官的内脏指数和生命延长率,同时设生理盐水组（空白对照组）和氟尿嘧啶组（阳性对照组）进行比较。结果：硫酸壳聚糖高、低剂量组和氟尿嘧啶组的抑瘤率分别为38.67%、30.19%和43.27%,3组的生命延长率分别为65.38%、69.23%和54.93%。和生理盐水组、氟尿嘧啶组相比,硫酸壳聚糖高、低剂量组的S180小鼠的胸腺指数均有明显增加（P〈0.05）。结论：硫酸壳聚糖能有效抑制S180小鼠肿瘤的生长和延长EAC小鼠的生存时间,其作用机制可能与其提高机体的免疫力有关。     

Effect of cannabinoids on neurotransmitter uptake,atpase activity and morphology of mouse brain synaptosomes

Δ¹-Tetrahydrocannabinol (Δ¹-THC) and cannabidiol (CBD), a psychoactive and a nonpsychoactive constituent of marijuana respectively, inhibit the uptake of ³H-labelled norepinephrine (NE), dopamine (DA), γ-aminobutyric acid (GABA) and serotonin (5-HT), by mouse brain synaptosomes. CBD is more effective than Δ¹-THC in the inhibition of neurotransmitter uptake. At 5 × 10^?5 M both CBD and Δ¹-THC inhibit uptake by 60–100%. The one exception to the above is the differential effect of Δ¹-THC and CBD on 5-HT uptake. At 10^?6 M of Δ¹-THC the uptake is twice that of the control value and at 5 × 10^?5 M uptake is still equal to control value. At the former concentration CBD has no effect on 5-HT uptake whereas at the latter concentration a 50 per cent inhibition is observed. Both Δ¹-THC and CBD inhibit Na⁺-K⁺-ATPase and Mg-ATPase activities; at 5 × 10^?5 M inhibition amounts to 40 per cent. Electron microscopy reveals that synaptosomal preparations are highly damaged at 5 × 10^?5 M. Thus inhibition of uptake could stem from either failure of ATPase activity, from disruption of synaptosomes, or from both.     

Oral carcinogenicity study with nickel sulfate hexahydrate in Fischer 344 rats

Until now, existing data on the oral carcinogenicity of nickel substances have been inconclusive. Yet, the assessment of oral carcinogenicity of nickel has serious scientific and regulatory implications. In the present study, nickel sulfate hexahydrate was administered daily to Fischer 344 rats by oral gavage for 2 years (104 weeks) at exposure levels of 10, 30 and 50 mg NiSO(4).6H(2)O/kg. This treatment produced a statistically significant reduction in body weight of male and female rats, compared to controls, in an exposure-related fashion at 30 and 50 mg/kg/day. An exposure-dependent increase in mortality was observed in female rats. However, the overall study survival rate (males and females) was at least 25 animals per group (compliant with OECD guidelines) in the treated animals. Daily oral administration of nickel sulfate hexahydrate did not produce an exposure-related increase in any common tumor type or an increase in any rare tumors. One tumor type was statistically increased in a nickel sulfate-treated group compared to the study controls (keratoacanthoma in the 10 mg NiSO(4).6H(2)O/kg/day males), but there was no exposure-response relationship for this common tumor type. This study achieved sufficient toxicity to reach the Maximum Tolerated Dose (MTD) while maintaining a sufficiently high survival rate to allow evaluation for carcinogenicity. The present study indicated that nickel sulfate hexahydrate does not have the potential to cause carcinogenicity by the oral route of exposure in the Fischer 344 rat. Data from this and other studies demonstrate that inhalation is the only route of exposure that might cause concern for cancer in association with nickel exposures.