安氟醚麻醉诱导Fos蛋白与脑啡肽在大鼠中枢神经系统的表达及定位研究

目的观察安氟醚麻醉后大鼠中枢神经系统各部位Fos蛋白与脑啡肽(ENK)的表达及共存情况.方法成年SD大鼠(第四军医大学实验动物中心提供)12只,雌雄不拘,体重195～223g,随机分为对照组和实验组,每组6只.实验组吸入2%安氟醚2h,对照组不吸入麻醉药,其余条件同实验组.经左心室灌注生理盐水100ml洗去全身血液,继之灌注含4%多聚甲醛的0.1mol/LPB500ml,固定90min,取全脑和脊髓冰冻连续冠状切片,双标记免疫组化染色,低倍光镜下观察染色阳性细胞的分布情况;高倍镜下观察鉴别Fos染色免疫阳性(FLI)细胞,ENK染色免疫阳性(ELI)细胞以及Fos、ENK共同表达(FLI/ELI)细胞,计数神经核团一个高倍视野内的阳性细胞数目.结果对照组中,ELI神经元较多,FLI神经元少量、散在无规律地分布,FLI/ELI神经元极少见.实验组中可明显观察到ELI、FLI、FLI/ELI三种神经元,主要分布在大脑额顶皮质、外侧隔核、杏仁核、海马CA1区、丘脑室旁核、丘脑腹外侧核、僵核、下丘脑腹内侧核、视上核、网状结构、脚间核、中脑中央灰质及脊髓背角等神经核团,这些核团内FLI和ELI神经元数量与对照组比较显著增多(P＜0.05),在其它核团内无显著变化;Fos、ENK双标神经元约占FLI神经元的15%～42%.结论安氟醚可诱导Fos蛋白在某些神经核团内表达并使其内ENK增多;Fos蛋白可能作为脑啡肽基因的转录调控因子,引起ENK的变化.     

亚低温对大鼠脑缺血再灌注损伤后Bcl- 2、Bax和C- fos蛋白表达及损伤神经细胞凋亡的影响

目的观察亚低温对大鼠脑缺血再灌注损伤后Bcl- 2、Bax和C- fos蛋白表达及损伤神经细胞凋亡的影响. 方法采用大鼠局灶性脑缺血再灌注损伤模型,大脑中动脉阻塞2 h,再灌注损伤6 h,用原位缺口末端标记(Tdtmediated dUTP- biotin nick end labeling,TUNEL)法和免疫组织化学法分别检测假手术组、对照组和亚低温组的凋亡细胞百分率和Bcl- 2、Bax和C- fos蛋白表达水平. 结果亚低温组Bcl- 2蛋白表达水平为(63.48±0.47)%,较对照组显著升高(P<0.05),而Bax和C- fos蛋白表达水平和凋亡细胞百分率分别为(6.13±0.93)%和(5.09±0.21)%,明显低于对照组(P<0.05). 结论亚低温下调大鼠脑缺血再灌注损伤后Bax和C- fos蛋白表达水平和上调Bcl- 2蛋白表达水平,可能与其抗损伤神经细胞凋亡作用有关.     

扶芳藤合剂预防给药对脑缺血后原癌基因C-fos表达的影响

目的观察扶芳藤、银杏叶合剂预防给药对局灶性脑缺血大鼠原癌基因C-fos表达的影响。方法采用免疫组化法检测大鼠脑缺血再灌注后不同时间点原癌基因C-fos表达的水平,观察各组实验大鼠脑缺血后C-fos表达水平的变化。结果大鼠脑缺血2h后再灌注不同时间点C-fos表达均升高,扶芳藤合剂预防给药可降低脑缺血再灌注后C-fos的表达。结论扶芳藤合剂预防给药,可能改善脑部血液循环,从而下调缺血脑组织C-fos蛋白表达,以减轻局灶性脑缺血后脑细胞的缺血性损伤。     

即刻早期基因c-fos与癫痫

c-fos作为即刻早期基因的一种，编码的Fos蛋白组成了其他许多基因的转录调控因子，因中将外界信号级联放大，造成细胞长期的生理功能改变。近年来，对c-fos进行了广泛而深入的研究，并取得了一定的成果。本文就其结果、功能及其与癫痫的关系作一综述。     

经牵涉皮区注入利多卡因对胃痛大鼠脊髓c-fos表达的影响

目的:探讨经胃牵涉皮区注入利多卡因对胃痛大鼠脊髓c-fos表达的影响及其意义。方法:在大鼠胃牵涉皮区皮下注入0.5%利多卡因2m l,10m in后,将2%甲醛溶液经胃管注入SD大鼠胃内,制成胃痛的大鼠模型;采用c-fos免疫组织化学技术,计数c-fos阳性细胞数,并与牵涉皮区内注入生理盐水组动物相比较。结果:牵涉皮区注入利多卡因组动物脊髓c-fos表达较其对照组显著减少(P<0.05)。结论:经牵涉皮区注入利多卡因后可能减轻胃痛信息的传导。     

地塞米松对缺氧缺血新生大鼠脑组织兴奋性氨基酸和C-fos蛋白表达的影响

目的观察地塞米松(DXM)对缺氧缺血新生大鼠脑组织兴奋性氨基酸(EAA)和C-fos蛋白表达的影响,探讨其在缺氧缺血性脑损伤(HIBD)中的应用价值。方法建立HIBD动物模型,应用高效毛细管电泳和免疫组化方法,分别检测假手术组、HIBD组、小剂量DXM干预组(0．5 mg/kg)及大剂量DXM干预组(10mg/kg)的脑组织EAA含量及C-fos蛋白表达水平。结果 HIBD组的EAA含量及C-fos蛋白表达均较假手术组明显升高(P<0．01);小剂量DXM组的EAA含量及C-fos蛋白表达较 HIBD组无明显变化(P>0．05);大剂量DXM组EAA含量较HIBD组明显减少(P<0．01),较小剂量 DXM组减少(P<0．05);大剂量DXM组C-fos蛋白表达较HIBD组及小剂量DXM组均明显降低(P< 0．01)。结论缺氧缺血促进脑组织EAA的释放,诱导C-fos蛋白表达;大剂量DXM干预可能通过抑制EAA释放,降低C-fos蛋白表达而对缺氧缺血脑损伤起保护作用。     

Neuroimmunological activation of the afferent laryngeal neural circuit in experimentally induced laryngeal inflammation

Conclusions These results show that laryngeal inflammatory reactions may induce the expression of proinflammatory cytokines along the afferent laryngeal circuit and in nuclei associated with the HPA axis. Local laryngeal inflammation may induce functional and physiologic alterations in the laryngeal neural system via neuroimmunologic reactions.

Objective Idiopathic laryngeal disorders associated with various neurologic conditions such as spasmodic dysphonia, idiopathic vocal fold paralysis and sudden infant death syndrome are causally related to upper respiratory tract infections, and it can be speculated that these disorders result in neurophysiologic alterations. The goal of this study was to identify the neurophysiologic effect on the central nervous system of local inflammatory alterations in the larynx.

Material and methods The expression of c-fos and IL-1β was identified after injecting saline solution, 10 μg of lipopolysaccharide or 100 μg of lipopolysaccharide into the larynx of 12 rats.

Results The inflammatory cytokine IL-1β was mainly expressed in the inferior olivary nucleus and raphe nucleus, which are associated with the hypothalamic–pituitary–adrenal (HPA) axis. IL-1β expression was also found in the nuclei of afferent nervous pathways of the superior laryngeal nerve, such as the nucleus tractus solitarius, nucleus ambiguus, lateral reticular nucleus, magnocellular reticular nucleus and paragigantocellular reticular nucleus.     

The oncoproteins c-erb-B2, c-fos and the tumour suppressor protein p53 in human embryos and fetuses

 Oncoproteins and tumour-suppressor proteins are thought to possess an antagonistic function in the regulation of growth and differentiation processes during embryonic and fetal development. In contrast, in the adult, tumour growth is associated with the overexpression of oncoproteins or the malfunction of tumour-suppressor proteins. We examined the occurrence of the tumour proteins c-erb-B2 and c-fos and the tumour-suppressor protein p53 in 17 human embryos and fetuses with the help of immunohistochemistry. C-erb-B2 was detected mainly in embryonic tissue that are not known for c-erb-B2-overexpression in tumours in the adult. In contrast, c-fos was almost always located in fetal tissues corresponding to its location in adult tumours. Staining for p53 was found in a wide variety of embryonic and fetal tissues. C-erb-B2 and p53 were localized in the same tissue structures of the developing skin, heart and muscle. In other tissues, e.g. muscle and bone, c-fos was found together with p53, suggesting an antagonistic action of these proliferative and antiproliferative factors. Furthermore, c-erb-B2, c-fos and p53 appear to be important for growth and differentiation processes in human development as the occurrence of these proteins was not only restricted to specific tissues but also to specific stages of development of these tissues. Accepted: 30 September 1996     

Gene expression in central cholinergic neurons in response to axotomy and deafferentation

Although the molecular and cellular responses to injury in the central nervous system (CNS) have been widely investigated, few studies have examined the potential variations between direct and indirect neuronal injury. To differentiate between the response to axotomy and deafferentation, two central cholinergic populations were analyzed: the horizontal limb of the diagonal band of Broca (HLDB) and the interneurons in the corpus striatum (CS). At time points from one hour to eight weeks postinjury the levels of choline acetyltransferase (ChAT) mRNA and protein were assessed by in situ hybridization and immunohistochemistry. Also examined was the expression of the immediate early gene product, c-fos. One week post axotomy, neurons in the HLDB exhibited an increase in the levels of ChAT mRNA without a concomitant increase in ChAT protein, followed by a steady decrease reaching a nadir in both parameters at eight weeks. In contrast, a transient increase occurred at one week postdeafferentation in the levels of both ChAT mRNA and protein in the interneurons of the CS. Axotomized neurons in the HLDB did not exhibit either c-fos mRNA or protein expression, while robust fos induction occurred after one hour in deafferented neurons in the CS. These data demonstrate that the molecular and cellular responses differ following direct and indirect neufenal injury. Furthermore, they suggest that in these central cholinergic populations deafferentation may result in cellular hyperactivity and cell survival while axotomy, results in decreased cellular activity and subsequent cellular regression. © 1994 Wiley-Liss, Inc.     

Alzheimer病模型大鼠类P3及其c-fos基因表达

目的 研究Alzheimer病(AD)大鼠类事件相关电位(类P3)及其c—fos基因的表达。方法 手术切断大鼠左侧穹窿—海马伞(FF)建立AD大鼠模型，于建模后1h、7d和15d对大鼠进行灌注固定，取含有海马结构的脑组织分别进行HE染色和Fos蛋白的免疫组化染色；并于建模前后分别进行电迷宫检查和类P3L测定．结果 ①AD大鼠类P3L显著延长于对照组，与迷宫试验指标EN，TRT呈正相关(r分别是0．78和0．51，P＜0．05)．②Fos样免疫活性在加大鼠的海马及大脑皮层均有增强，并随术后时间的延长而不断增强。结论 ①手术切断FF所建AD模型可以由拟出与加患者类似的P3L延长和c—fos过度表达．②建模后，AD大鼠类P3L延长与Fos—LI增强呈正相关趋势。