人参皂苷Rg_1对大鼠海马c-fos基因表达和cAMP含量的影响(英文)

目的:探讨Rg_1对神经系统作用的机制。方法:采用Northern和Western印迹分析法,检测了Rg_1处理前后大鼠海马组织的c-fos基因和蛋白的表达。结果:老年鼠c-fos基因和蛋白的表达明显低于青年鼠,但给Rg_1后老年鼠和青年鼠均呈现显著性增强效应。此外,Rg_1还明显增加青年鼠和老年鼠海马组织的cAMP含量。结论:Rg_1升高cAMP水平及促进c-fos基因和蛋白的表达有助于阐明其促智和抗衰老作用的机制。     

血管紧张素-（1-7）抑制肾小球系膜细胞增殖过程中c-fos蛋白表达

目的观察血管紧张素-（1-7）[Ang-（1-7）]对血管紧张素-Ⅱ（Ang-Ⅱ）诱导的肾小球系膜细胞（GMC）增殖过程中c-fos表达的影响。方法体外培养GMC，Ang-Ⅱ为刺激因子，不同浓度Ang-（1-7）为干预因子。用结晶紫计数法检测GMC数目的变化；Western blot检测GMC中c-fos蛋白表达的变化。结果Ang-（1-7）呈剂量依赖性地抑制Ang-Ⅱ诱导的GMC增殖和GMC内c-fos蛋白表达。结论Ang-（1-7）可能通过抑制c-fos的表达，抑制Ang-Ⅱ诱导的GMC增殖。     

一氧化氮对胃癌细胞AGS 生长的抑制及其机制探讨*

目的:探讨外源一氧化氮（nitric oxide,NO）对胃癌AGS 细胞生长及c-jun和c-fos表达的影响。方法:应用MTT 法评价NO供体硝普钠（sodium nitroprusside,SNP ）,SNP 的同源类似物铁氰化钠Na3Fe（CN）6 和一氧化氮合酶（nitric oxide synthase,NOS ）抑制剂N-硝基-L- 精氨酸甲酯（N-nitro-L-arginine methylester ,L-NAME ）对胃癌细胞生长的抑制作用,RT-PCR 和免疫印迹检测c-jun和c-fos的基因和蛋白表达。结果:SNP 剂量依赖性的抑制AGS 细胞的生长,其IC 50值为2.13mmol/L 。1mmol/L SNP 处理12、24、48h 后,细胞生长抑制率分别为（16.12± 0.85）% 、（20.33± 1.31）% 、（22.06± 2.03）%（P<0.05）,NOS 抑制剂L-NAME 预处理明显减弱了SNP 对癌细胞的生长抑制效应,Na3Fe（CN）6 对胃癌细胞生长无抑制。与对照组比较,SNP 使c-jun和c-fos的mRNA 和蛋白表达降低,NOS 抑制剂L-NAME 预处理逆转了SNP 的这种作用,Na3Fe（CN）6 对c-jun和c-fos的mRNA 和蛋白表达无影响。结论:NO可诱导胃癌细胞c-jun和c-fos表达降低,抑制癌细胞生长。      

孕酮对牙周膜成纤维细胞c—los、c-jun基因表达的影响

目的：研究孕酮对牙周膜成纤维细胞c—fos、c-jun基因表达的影响,探讨孕酮促进人牙周膜成纤维细胞（hPDLCs）增殖和成骨分化的可能机制。方法：原代培养hPDLCs,取第4-6代细胞用于实验。分为空白对照组,孕酮组,抑制剂组。各组细胞培养2h,采用反转录聚合酶链反应检测c—fos和c-junmRNA的表达。结果：RT—PCR的结果说明,孕酮能促进c—fos和c-junmRNA的表达,抑制剂组c—fos和c-junmRNA的表达下调。结论：孕酮能够上调hPDLCs中c—fos、c-jun的表达。提示孕酮可能通过上调c—fos、c-jun的表达促进hPDLCs的增殖和成骨分化,促进骨形成。     

GCS对急性炎性大鼠脑内c-fos表达的影响

目的 为探讨糖皮质激素(GCS)对脑内神经细胞的作用提供形态学资料.方法 动物行为学观察、免疫组化法神经细胞染色和形态计量学方法.结果 在大鼠后爪掌面皮下注射2.5%甲醛20μl可造成注射处急性持续性炎症.1h后,双侧中缝大核、丘脑、大脑皮层fos样免疫阳性神经元总数明显上升.用地塞米松预处理2h后可使相应部位FLI神经元数明显降低,具有剂量依赖性.外周水肿、疼痛表现与脑内FLI细胞数呈正相关.用糖皮质激素受体阻断剂RU486可部分反转GCS的效应.结论 ①伤害性刺激可引起中枢神经系统c-fos广泛表达;②GCS对中枢神经元c-fos表达的效应有差异性.     

绞股蓝总皂苷对全脑缺血再灌注大鼠海马区c-fos蛋白表达的影响

【目的】探讨绞股蓝总皂苷(gypenosides,GP)对全脑缺血再灌注大鼠海马区c-fos蛋白表达的影响。【方法】用改良的Pulsinelli 4-血管阻断(4-VO)法制做大鼠急性全脑缺血再灌注损伤模型,分别按照再灌注6、24、72 h取材,应用免疫组织化学染色法标记各实验组大鼠脑组织海马区c-fos蛋白表达数量。【结果】与对照组比较,模型组JUN蛋白表达最高。各组海马区的JUN蛋白表达随着缺血再灌注时间的延长逐渐减少(再灌注6 h>再灌注24 h>再灌注72 h)。与模型组相比,绞股蓝总皂苷2个剂量组在不同灌注时间(6、24、72 h)均具有显著的抑制FOS蛋白表达的作用。【结论】绞股蓝总皂苷可明显下调FOS蛋白的表达,具有抑制全脑脑缺血再灌注时神经细胞凋亡作用,从而改善受损的神经功能。GP对急性全脑缺血模型大鼠的脑损伤的预防保护有一定的剂量相关趋势,GP高剂量给药组保护效果好于GP低剂量给药组。     

The mechanism of growth-regulation of glioma cells by trapidil

Summary Trapidil is a PDGF antagonist that can inhibit the proliferation of the PDGF-producing glioma cells, U251MG. As the mechanism of growth-regulation by trapidil remains unclear, we studied its effect on the growth of U251MG cells. We performed a cell cycle analysis and examined the intracellular transduction pathway and oncogene expression in serum-stimulated glioma cells with or without trapidil.After the serum starvation for 3 days, glioma cell proliferation was stimulated by the addition of serum. Cell cycle analysis showed that cell cycle perturbations induced by trapidil included a decreased transition rate from G₀-G₁ to S phase, suggesting that some metabolic event is required for progress through the G₀-G₁ phase and that this event is sensitive to trapidil. Internal signal transduction mechanisms are central in the molecular control of cell growth. One such regulator is the protein kinase C(PKC) system and the c-fos gene is likely to be a direct target of intracellular signal transduction pathways. Therefore, we hypothesize that the intracellular PKC activity and c-fos expression of the trapidil-treated cells are suppressed. We posit that trapidil affects the intracellular signal transduction pathway PKC activity and c-fos expression in cells stimulated with serum containing growth factors.     

Neuroanatomical substrates involved in the anxiogenic-like effect of acute fluoxetine treatment

An initial exacerbation of anxiety can be observed in animals and humans treated with selective serotonin reuptake inhibitors (SSRIs). The neurobiological substrates and mechanism(s) underlying this effect are not clear. We used Fos expression as a marker of neuronal activation to investigate effects of acute fluoxetine treatment in rats submitted to two different models of emotional stress, airjet and immobilization. Exposure to both stressors induced Fos expression in various brain regions implicated in fear/anxiety mechanisms. Acute treatment with 5 mg/kg fluoxetine facilitated airjet-induced escape responses and enhanced the airjet-, as well as immobilization-induced Fos expression exclusively in the locus coeruleus (LC), but not in other areas including the amygdala, hypothalamus or septum. Fluoxetine also facilitated airjet-induced noradrenaline efflux in the medial prefrontal cortex, a projection area of LC noradrenergic neurons. A higher dose of fluoxetine (10 mg/kg) did not change escape responses and had no effect on stress-induced Fos expression in the LC, but decreased airjet-induced Fos expression in the medial amygdala. The results indicate that anxiogenic effects of acute fluoxetine treatment occur in a specific dose range and can be mimicked by exacerbation of escape responses in the airjet model. Furthermore, facilitation of escape responses by fluoxetine is linked to enhanced activity in the LC/noradrenaline system.