双胸蚓溶栓酶对胎鼠大脑皮层神经细胞生长发育的作用

为探讨双胸蚓溶栓酶对神经细胞的影响及其作用机制，我们应用神经细胞体外培养技术观察了１至３０日内在不同剂量双胸蚓溶栓酶作用下的Ｗｉｓｔａｒ胎鼠大脑神经细胞的生长发育过程。结果显示：不同剂量双胸蚓溶栓酶对神经细胞突起的数量和长度以及轴索的形成与增长均有影响。表明双胸蚓溶栓酶对体外培养的胎鼠大脑神经细胞的生长发育有促进作用     

双胸蚯蚓溶栓酶对体外培养大脑神经细胞的影响

以体外培养的大白鼠大脑皮层神经细胞为实验材料，在不同时程内，通过观察细胞生长状态和突起长度以及测定培养液中肌酸激酶的活性，探讨双胸蚯蚓溶栓酶对大脑神经细胞的影响。结果表明，实验组细胞长势、突起长度以及培养液中肌酸激酶的活性均优于对照组，差异显著。提示该酶对大脑神经细胞具有保护和促进生长的作用。     

人胎脊髓内源性物质对脊髓中GABA神经元的营养作用

目的:从人胎脊髓提取液中寻找对脊髓GABA神经元有神经营养作用的成分。方法:用四月龄人胎制备脊髓提取液,加人体外培养的胎鼠脊髓细胞中,观察提取液对神经元活性、突起生长和分化的影响。结果:人胎脊髓中有提高GABA神经元活性的营养成分,并且小于10kD组分还可以诱导GABA神经元的分化,但是提取液对GABA神经元的突起生长没有影响。结论:实验结果揭示人胎脊髓中可能存在不止一种神经营养活性成分,对GABA神经元的活性和分化起营养作用。     

神经生长因子对体外培养大脑基底神经节神经元的保护作用

目的:研究神经生长因子(NGF)对谷氨酸造成的体外培养大脑基底神经节神经元损伤后的再生及防止神经元坏死的保护作用。方法:原代培养的胎鼠前脑基底神经节神经元,分为对照组、谷氨酸损伤组和谷氨酸损伤后NGF保护组。用倒置相差显微镜进行活细胞观察、采用RT-PCR技术检测前脑基底神经节神经元GAP-43和NF-L基因表达。结果:谷氨酸损伤神经元胞体回缩,突起消失或断裂。加入NGF后神经元绝大多数细胞胞体饱满,突起明显,细胞问的网络联系清晰可见,接近于对照组;NGF保护组大脑基底神经节GAP-43 mRNA和NF-L mRNA表达与损伤组比较具有显著性差异。结论:NGF可保护谷氨酸造成体外培养的大脑基底神经节损伤后的再生,并防止神经元坏死。     

双胸蚓溶栓酶抗实验性缺血性脑损伤的作用

为寻求双胸蚓溶栓酶抗缺血后再灌流脑损伤的作用，夹闭沙土鼠双侧颈总动脉颈前脑缺血再灌流性脑损伤。用ＨＲＰ逆行追踪法在光镜下观察丘脑内标记细胞。结果表明：实验组１５例１５０张切片中丘脑标记细胞总数为２２２１个，平均每张切片为１４．８个，对照组１５例１５０例张片中生脑标记细胞总数为８３８个，平均为５．５９个，两组丘脑内各核群标记细胞的数量差异非常显著。说明双胸蚓溶栓酶对缺血后损伤的脑组织有明显的保护作用     

银杏内酯对大鼠基底前脑神经元生长发育的影响

目的：观察银杏内酯对培养的胚胎大鼠基底前脑胆碱能神经元和NADPH-d阳性神经元生长发育的作用。方法：取E17Wistar大鼠胚胎基底前脑进行体外细胞培养，并给予银杏内酯。进行乙酰胆碱酯酶(acetyl cholinesterase，AChE)和NADPH-d酶组织化学染色，并在光镜下进行阳性细胞计数和显微测量胞体及突起发育状况。结果：给予银杏内酯处理后，培养物中乙酰胆碱酯酶阳性神经元和NADPH-d阳性神经元数量均较对照组显著增加，且神经元发育状况好于对照组，胞体大，突起多且长。结论：银杏内酯可以促进体外培养的基底前脑神经元中乙酰胆碱酯酶和NADPH-d的表达，并能促进表达这两种酶的神经元生长发育。     

神经节苷脂对损伤胎鼠背根神经节的保护作用

目的观察神经节苷脂(GM1)对受损伤胎鼠背根神经节(DRG)神经元形态改变的影响,探讨其可能的保护作用。方法选择胎龄为15d的SD大鼠为研究对象,获取DRG神经元并进行体外分散培养,培养48h后,随机分为对照组、谷氨酸损伤组和谷氨酸损伤+GM1保护组,继续培养12h。终止培养后,观察各组神经元的形态结构改变,用MTT法鉴定细胞的存活率。结果对照组DRG神经元细胞贴壁呈单层散在分布,少部分出现细胞聚集现象,突起较长且互相交织形成网状。谷氨酸损伤组DRG神经元细胞聚集现象明显,神经元突起变短、断裂甚至消失。谷氨酸损伤+GM1保护组DRG神经元细胞部分呈簇状聚集,部分呈单个散在分布,突起仍然相互交织。MTT结果显示谷氨酸损伤+GM1保护组细胞存活率高于谷氨酸损伤组。结论神经节苷脂可以影响损伤胎鼠DRG神经元的形态改变,对胎鼠背根神经节神经元具有一定的保护作用。     

BDNF、NGF对体外培养的胚胆碱能神经元生长发育的影响

本文用AChE组化方法，研究了BDNF、NGF对培养的胚鼠基底前脑胆碱能神经元的作用及BDNF和NGF的协同作用。结果表明BDNF和NGF都具有增加AChE阳性神经元数量的作用，二者的不同在于BDNF作用出现的时间较早、强度较小；而NGF作用出现的时间较迟但强度较大。并发现BDNF对体外培养的胚胆碱能神经元胞体早期的生长发育作用比较明显，而NGF的作用则不甚显著。BDNF对胚胆碱能神经元发出突起和突起的延伸作用较NGF强。BDNF和NGF的联合作用较单独使用BDNF或NGF为好。本文的结果提示在体外培养中两种营养因子联合应用较只用一种因子有益。     

双胸蚯蚓溶栓酶对沙土鼠缺血额叶皮质超微结构及离子的影响

采用结结扎沙土鼠双颈总动脉２０分钟后恢复血流制作脑缺血再灌注模型，应用透射电镜对额叶皮超微结构进行观察，并采用电镜能谱技术对神经元随机检测Ｎａ＾＋，Ｃａ离子含量，探讨双胸蚯蚓溶栓酶对额叶皮质神经元的影响，结果：缺血的对照组神经元Ｎａ＾＋明增高达１６．４３，而缺血后腹腔注入双胸蚯蚓溶栓酶的实验组显著下降为１３．０２，接近正常组的１１．４７，Ｃａ正常组为１．０３，对照组增高达３．８１，而实验组下降为２     

Neurturin对体外培养的GABA阳性神经元生长发育的作用

为探讨neurturin(NRTN)、神经生长因子(NGF)对新生大鼠海马的γ氨基丁酸能神经元生长发育的影响,本研究用免疫组化结合图像分析技术观察neurturin和NGF对体外培养海马的γ氨基丁酸能阳性神经元生长发育的作用。结果显示:培养4d时,NRTN组的γ氨基丁酸能阳性神经元细胞数目、突起数、胞体面积和最长突起长度均与对照组有显著性差异(P<0.05),NGF组各项指标与对照组均无显著性差异(P>0.05),NGF+NRTN组突起数多于NRTN组(P<0.05);培养8 d时,NRTN组各项指标均与对照组仍有明显差异(P<0.05),NGF+NRTN组突起数仍多于NRTN组(P>0.05)。上述结果提示,neurturin对体外培养的新生大鼠γ氨基丁酸能阳性神经元生长发育有营养作用,但NGF对体外培养的新生大鼠γ氨基丁酸能阳性神经元无神经营养作用;neurturin和NGF的联合应用并不比单独使用neurturin好。     

Tactivin in the regulation of dexamethasone-induced apoptosis in thymocytes

The level of natural apoptosis in rat thymus on day 18 of embryo development attained 25%, while at subsequent terms it was about 5%. In the spleen, this parameter gradually decreased from 15 to 37% starting from day 18 of embryo development to postnatal day 30. Tactivin prevented the development of dexamethasone-induced apoptosis in thymocytes of 30-day-old rats, but had no effect on spontaneous apoptosis. Tactivin can be used as a modulator of apoptotic processes. __________ Translated from Byulleten’ Eksperimental’noi Biologii i Meditsiny, Supplement 2, pp. 109–111, April, 2007     

二恶英对成骨细胞胰岛素样生长因子家族基因表达的抗雌激素作用

目的 探讨大鼠骨骼发育过程中环境类致畸因子对成骨细胞中胰岛索样生长因子(insulin-like growth factors，IGFs)家族基因表达的抗雌激素作用。方法 应用环境类致畸因子二恶英(2，3，7，8-tetrachlorodibenzo—p—dioxin，TCDD)构建先天性大鼠骨骼发育畸形动物模型；应用雌激素和TCDD分别或联合作用于小鼠头盖骨成骨样(MC-3T3-E1)细胞株；再用逆转录-聚合酶链反应及流式细胞仪定量检测胎鼠头盖骨组织和MC-3T3-E1细胞中IGF—I和胰岛索样生长因子结合蛋白-6(insulin—like growth factor binding protein-6，IGFBP-6)mRNA的表达和细胞增殖率。结果 在5～15μg／kgTCDD浓度下诱导了大鼠骨骼发育畸形，并存在剂量依赖性生物学效应；雌激素增加了胎鼠头盖骨组织及MC-3T3-E1细胞中IGF—ImRNA的表达，提高了MC-3T3-E1细胞的增殖率，但使IGFBP-6mRNA的表达降低；TCDD抑制了雌激素对IGF—I、IGFBP-6基因表达及细胞增殖的调节作用。结论 在高雌激素水平下，TCDD可以诱导大鼠骨骼发育畸形；通过靶基因IGF—I和IGFBP-6，TCDD可发挥拮抗雌激素对成骨细胞的正性调节作用。     

前列腺素E受体1在缺氧性神经细胞死亡中的作用

目的:探讨前列腺素E受体1(EP1)在缺氧性神经细胞死亡中的作用。方法:采用原代培养的大鼠出生24h内的大鼠子鼠皮质神经细胞,给予缺氧再给氧处理,用噻唑蓝比色法(MTT)测定神经细胞生存率,流式细胞技术测定细胞凋亡率,用Western印迹法检测caspase-3蛋白质的表达。结果:EP1激动剂17-pt能明显降低缺氧再给氧后神经细胞的生存率,细胞生存率呈浓度依赖性,17-pt预处理组与单纯缺氧再给氧组相比,17-pt能明显增加由于缺氧而引起的细胞死亡率,细胞凋亡率增高,caspase-3蛋白质表达量增加(P0.05)。结论:EP1参与了缺氧缺血后神经细胞死亡的病理过程,有可能成为缺血性中风治疗的新分子靶点。     

Electron microscopical and enzyme histochemical investigation of kidney and liver of the albino rat after cytostatic treatment (author's transl)]

Within 5 days following treatment with cytostatics (vincristine, vinblastine, trenimon, 5-fluorouracil) enzyme-histochemical and ultrastructural changes occurred in the kidney and liver of Wistar rats. The enzyme activities were influenzed by cytostatics in different ways. It was found that the activity of some enzymes increased whereas that of others decreased. Kidney and liver showed a different response in their enzymatic behaviour. The cytostatics used did not have the same effect. The histochemical changes following injection of cytostatics in juvenile rats do not agree with those in adult ones. The electronmicroscopic findings reveal marked morphological changes of the kidney and liver cells within the first 5 days following injection of cytostatics. From the 8th day on after administration of cytostatics neither histochemical nor ultrastructural changes as compared with the controlls were found.     

Effect of enzyme imprinting of liver microsomal monooxygenases upon lifespan of rats.

Effect of the enzyme imprinting by phenobarbital upon alterations of hepatic microsomal monooxygenase activities and lifespan of Wistar rats has been studied. Phenobarbital-sodium (3.5 mg/100 g body weight per day, i.p.) was injected during 1-3 days after birth. This resulted in the enzyme imprinting of the liver microsomal monooxygenases, however, this effect being observed in female but not male rats. In the phenobarbital treated female rats of different age the duration of sleeping time was significantly lower than that in control animals, whereas it did not differ substantially in male rats. The cytochrome P-450 content increased by 34.5% in phenobarbital treated female rats in the age of 12 months in comparison with control animals. A mean lifespan of experimental female rats increased by 17.5% compared to the level of control animals and did not change in male rats. The analysis of survival of animals in Gompertz equation coordinates showed that enzyme imprinting by phenobarbital caused changes in the mortality patterns at different stages of ontogenesis in experimental female but not male rats. An inverse correlation was found between the duration of pentobarbital sleeping time and lifespan of female and male rats.     

Age-dependent changes of morphometric and histochemical characteristics of neurocytes in different ganglia of albino rats

The aim of this study was to obtain the normative data on the age-dependent transformation of morphometric and histochemical characteristics of neurocytes in different ganglia in albino rats. Cell cross-sectional area, activities of cholinesterase (demonstrated with thioacetic acid method) monoamine oxidase (demonstrated with Glenner method) were measured in neurocytes of stellate, spinal, trigeminal and gastric ganglia in rats aged 2 to 360 days. Measurements were made with the help of "Bioscan" videoanalyzer. Informational analysis was used for the evaluation of the degree of maturation of neurocyte systems. General features, age- and organ-related peculiarities of morphometric and enzyme-histochemical characteristics were established for neurocytes of different ganglia, as well as a heterochronism of their definitive state attainment. The time of stabilization for neurocytes of stellate and I thoracic spinal ganglia was the age of 60 days, for those of trigeminal ganglion and intramural gastric ganglia -90 and 120 days, respectively. By this time, neurocyte systems turned from a determined state into a probabilistic-determined one, this transformation being considered as a population stabilization.     

碘缺乏对大鼠大脑锥体细胞的影响

目的：探讨缺碘在地方性克汀病发病机制中的作用。方法：通过低碘饲料和补碘饲料喂养母鼠，分娩的仔鼠40d龄时开始实验．观察仔鼠脑发育的变化：结果：低碘组大鼠锥体细胞顶树突棘突密度、棘突的分布类型、锥体细胞基树突数和初级树突分枝指数及锥体细胞的最大横截面积与加碘组大鼠和对照组大鼠均有显著性差异。结论：低碘饮食使大鼠锥体细胞各方面的生长、发育受到抑制．妊娠前补充碘可弥补缺碘对中枢神经系统发育的损害作用。