Expression of a fusion protein of human ciliary neurotrophic factor and soluble CNTF-Receptor and identification of its activity

Ciliary neurotrophic factor (CNTF) has pleiotropic actions on many neuronal populations as well as on glia. Signal transduction by CNTF requires that it bind first to CNTF R, permitting the recruitment of gp130 and LIF R, forming a tripartite receptor complex. Cells that only express gp130 and LIF R, but not CNTF R are refractory to stimulation by CNTF. On many target cells CNTF only acts in the presence of its specific agonistic soluble receptors. We engineered a soluble fusion protein by linking the COOH terminus of sCNTF R to the NH 2 terminus of CNTF. Recombinant CNTF/sCNTF R fusion protein (Hyper CNTF) was successfully expressed in COS 7 cells. The apparent molecular mass of the Hyper CNTF protein was estimated from western blots to be 75 kDa. Proliferation assays of transfected BAF/3 cells in response to CNTF and Hyper CNTF were used to verify the activity of the cytokines. The proliferative results confirmed that CNTF required homodimerization of the gp130, CNTF R and LIF R receptor subunit whereas Hyper CNTF required heterodimerization of the gp130 and LIF R receptor subunit. We concluded that the fusion protein Hyper CNTF had superagonistic activity on target cells expressing gp130 and LIF R, but lacking membrane bound CNTF R.

Effect of ciliary neurotrophic factor on activation of astrocytes in vitro

Objective To observe the activating effect of ciliary neurotrophic factor （CNTF） on astrocyte in vitro. Methods Astrocytes cultured purely from newborn rats. Cerebral cortex was raised in normal and serum deprivation condition with different concentrations （in ng/ml： 0, 2, 20, or 200） of CNTF. After cultured for 24 h, the shape and the cell cycle of astrocytes were examined by immunocytochemistry and flow cytometer, respectively. Results The immunoactivity of glial fibrillary acidic protein （GFAP） and the nuclear size of astrocytes were increased when CNTF was applied, whether cells were cultured in medium with or without serum. CNTF promoted astrocytes to enter the cell cycle in medium with serum, but had no this effect in medium without serum. Conclusion In medium without serum, astrocytes could differentiate into activated state ceils with CNTF application, but could not proliferate; in medium with serum, astrocytes could proliferate with aid of CNTF.

Chemically extracted acellular allogeneic nerve graft combined with ciliary neurotrophic factor promotes sciatic nerve repair

A chemically extracted acellular allogeneic nerve graft can reduce postoperative immune rejection, similar to an autologous nerve graft, and can guide neural regeneration. However, it remains poorly understood whether a chemically extracted acellular allogeneic nerve graft combined with neurotrophic factors provides a good local environment for neural regeneration. This study investigated the repair of injured rat sciatic nerve using a chemically extracted acellular allogeneic nerve graft combined with ciliary neurotrophic factor. An autologous nerve anastomosis group and a chemical acellular allogeneic nerve bridging group were prepared as controls. At 8 weeks after repair, sciatic functional index, evoked potential amplitude of the soleus muscle, triceps wet weight recovery rate, total number of myelinated nerve fibers and myelin sheath thickness were measured. For these indices, values in the three groups showed the autologous nerve anastomosis group 〉 chemically extracted acellular nerve graft ＋ ciliary neurotrophic factor group 〉 chemical acellular allogeneic nerve bridging group. These results suggest that chemically extracted acellular nerve grafts combined with ciliary neurotrophic factor can repair sciatic nerve defects, and that this repair is inferior to autologous nerve anastomosis, but superior to chemically extracted acellular allogeneic nerve bridging alone.

Biomechanical analysis of optic nerve injury treated by compound light granules and ciliary neurotrophic factor

In this study, rabbit models of optic nerve injury were reproduced by the clamp method. After modeling, rabbit models were given one injection of 50 ng recombinant human ciliary neurotrophic factor into the vitreous body and/or intragastric injection of 4 g/kg compound light granules containing Radix Angelicae Sinensis and Raidix Paeoniae Alba at 4 days after modeling, once per day for 30 consecutive days. After administration, the animals were sacrificed and the intraorbital optic nerve was harvested. Hematoxylin-eosin staining revealed that the injured optic nerve was thinner and optic nerve fibers were irregular. After treatment with recombinant human ciliary neurotrophic factor, the arrangement of optic nerve fibers was disordered but they were not markedly thinner. After treatment with compound light granules, the arrangement of optic nerve fibers was slightly disordered and their structure was intact. After combined treatment with recombinant human ciliary neurotrophic factor and compound light granules, the arrangement of optic nerve fibers was slightly disordered and the degree of injury was less than after either treatment alone. Results of tensile mechanical testing of the optic nerve showed that the tensile elastic limit strain, elastic limit stress, maximum stress and maximum strain of the injured optic nerve were significantly lower than the normal optic nerve. After treatment with recombinant human ciliary neurotrophic factor and/or compound light granules, the tensile elastic limit strain, elastic limit stress, maximum stress and maximum strain of the injured optic nerve were significantly increased, especially after the combined treatment. These experimental findings indicate that compound light granules and ciliary neurotrophic factor can alleviate optic nerve injury at the histological and biochemical levels, and the combined treatment is more effective than either treatment alone.

Protective effects of ciliary neurotrophic factor on the retinal ganglion cells by injure of hydrogen peroxide

AIM： To explore the effect of ciliary neurotrophic factor （CNTF） on retinal ganglion cell （RGC）-5 induced by hydrogen peroxide （H2O2）. METHODS： After cell adherence, RGC-5 culture medium was changed to contain different concentrations of H2O2 from 50 to 150 μmol/L at four time points （0.5, 1, 1.5 and 2h） to select the concentration and time point for H2O2 induced model. Two different ways of interventions for injured RGC-5 cells respectively were CNTF as an addition in the culture medium or recombinant lentiviral plasmid carrying CNTF gene transfecting bone mesenchymal stem cells （BMSCs） for co-culture with RGC-5. RESULTS： Compared to the control group, H2O2 led to RGC-5 death closely associated with concentrations and action time of H2O2 and we chose 125 μmol/L and 2h to establish the H2O2-induced model. While CNTF inhibited the loss of RGC-5 cells obviously with a dose-dependent survival rate. Nevertheless two administration routes had different survival rate yet higher rate in recombinant lentiviral plasmid group but there were no statistically significant differences. CONCLUSION： Both the two administration routes of CNTF have effects on RGC-5 cells induced by H2O2. If their own advantages were combined, there may be a better administration route.

Influence of endogenous ciliary neurotrophic factor on neural differentiation of adult rat hippocampal progenitors

Ciliary neurotrophic factor is the only known neurotrophic factor that can promote differentiation of hippocampal neural progenitor cells to glial cells and neurons in adult rats. This process is similar to spontaneous differentiation. Therefore, ciliary neurotrophic factor may be involved in spontaneous differentiation of neural stem cells. To verify this hypothesis, the present study isolated neural progenitor cells from adult male rats and cultured them in vitro. Results showed that when neural progenitor cells were cultured in the absence of mitogen fibroblast growth factor-2 or epidermal growth factor, they underwent spontaneous differentiation into neurons and glial cells. Western blot and immunocytochemical staining showed that exogenous ciliary neurotrophic factor strongly induced adult hippocampal progenitor cells to differentiate into neurons and glial cells. Moreover, passage 4 adult hippocampal progenitor cells expressed high levels of endogenous ciliary neurotrophic factor, and a neutralizing antibody against ciliary neurotrophic factor prevented the spontaneous neuronal and glial differentiation of adult hippocampal progenitor cells. These results suggest that the spontaneous differentiation of adult hippocampal progenitor cells is mediated partially by endogenous ciliary neurotrophic factor.

In vitro neuroprotective effects of ciliary neurotrophic factor on dorsal root ganglion neurons with glutamate-induced neurotoxicity

Ciliary neurotrophic factor has neuroprotective effects mediated through signal transducer and Janus kinase（JAK） 2/activator of transcription 3（STAT3） and phosphatidylinositol 3-kinase（PI3 K）/Akt signaling pathways.Whether ciliary neurotrophic factor is neuroprotective for glutamate-induced excitotoxicity of dorsal root ganglion neurons is poorly understood.In the present study,the in vitro neuroprotective effects of ciliary neurotrophic factor against glutamate-induced excitotoxicity were determined in a primary culture of dorsal root ganglion neurons from Wistar rat embryos at embryonic day 15.Whether the JAK2/STAT3 and PI3 K/Akt signaling pathways were related to the protective effects of ciliary neurotrophic factor was also determined.Glutamate exposure inhibited neurite outgrowth,cell viability,and growth-associated protein 43 expression and promoted apoptotic neuronal cell death,all of which were reversed by the administration of exogenous ciliary neurotrophic factor.Additionally,preincubation with either JAK2 inhibitor AG490 or PI3 K inhibitor LY294002 blocked the neuroprotective effect of ciliary neurotrophic factor.These data indicate that the two pathways JAK2/STAT3 and PI3 K/Akt play major roles in mediating the in vitro neuroprotective effects of ciliary neurotrophic factor on dorsal root ganglion neurons with glutamate-induced neurotoxicity.

Effect of ciliary neurotrophic factor on bcl-2 and c-jun gene and protein expression in cultured retinal nerve cells

BACKGROUND：In various retinal neurodegenerative animal models,ciliary neurotrophic factor （CNTF） exhibits prominent neuroprotective effects on retinal nerve cells.Bcl-2 is an anti-apoptotic protein.c-Jun is upregulated and phosphorylated in the activated c-Jun N-terminal kinase pathway,which subsequently mediates apoptosis.However,the effect of CNTF on Bcl-2 and c-Jun expression in retinal nerve cells remains unclear.OBJECTIVE：To determine the dynamic changes in retinal nerve cell apoptosis,as well as bcl-2 and c-jun gene and protein expression,following a single dose of CNTF in a short period of time.DESIGN,TIME AND SETTING：A single-blind,randomized,controlled,in vitro experiment was performed at the Central Laboratory of Beijing Tongren Hospital from May 2008 to April 2009.MATERIALS：Neonatal bovine retinal nerve cells （Chinese Holstein）,recombinant human CNTF （PeproTech,Rocky Hill,NJ,USA）,rabbit polyclonal anti-Bcl-2 and c-Jun antibodies （Abeam,Cambridge,UK）,fluorescein isothiocyanate-conjugated annexin V/propidium iodide kit （BioVision,Mountain View,CA,USA）,real time polymerase chain reaction instrument （ABI,Foster City,CA,USA）,and flow cytometer （BD FACSCalibur,Franklin Lakes,NJ,USA）.METHODS：Neonatal bovine retinal cells from passage 2 were cultured for 3 days and incubated with,or without,50 ng/mL CNTF （control）.MAIN OUTCOME MEASURES：Cell apoptosis was detected via Annexin V-FITC/PI double-staining and flow cytometry.bcl-2 and c-jun mRNA and protein expression were detected by quantitative real time polymerase chain reaction and western blot analysis.RESULTS：The proportion of late-stage apoptotic cells was significantly decreased at 2,4,and 6 days after CNTF treatment compared with the control group （P 〈 0.01）.CNTF did not alter bcl-2 mRNA expression at the three time points,but significantly increased Bcl-2 protein expression at 2 and 4 days （P 〈 0.01）.c-jun mRNA expression was significantly decreased 4 days after CNTF treatment （P〈 0.01）.In addition,c-Jun protein expression was slightly increased at 4 days （P〈 0.01）,but decreased at 6 days,compared with the control group （P〈 0.05）.CONCLUSION：A single dose of CNTF （50 ng/mL） upregulated Bcl-2 protein and downregulated c-jun mRNA expression,followed by a parallel,but lagged,change in c-Jun protein production in cultured neonatal bovine retinal nerve cells.These results suggested that CNTF reduces retinal nerve cell apoptosis by modifying Bcl-2 and c-Jun expression.

Inhibition of ciliary neurotrophic factor in a rat model of transected spinal cord

Ciliary neurotrophic factor （CNTF） dramatically increases following spinal cord injury and participates in the repair process, although some studies have shown that CNTF plays a role in promoting glial scar formation following spinal cord injury. The antibody closure model can be used to inhibit CNTF expression following spinal cord injury, thereby furthering the understanding of the role of CNTF in spinal cord injury repair. In the present experiment, spinal catheters were placed in the vertebral canal of spinal cord transected rats, and CNTF antibodies were injected following fixation of the paraspinal muscle catheter. At 24 hours after a single CNTF antibody injection, CNTF expression decreased in the thoracic and lumbar spinal cord and recovered to normal levels by 48 72 hours. CNTF antibody treatment can effectively block endogenous CNTF expression in the thoracic and lumbar spinal cord during an interval of less than 24 hours in transected rats.

Induction of Differentiation of Mesenchymal Stem Cells into Retinal Pigment Epithelial Cells for Retinal Regeneration by Using Ciliary Neurotrophic Factor in Diabetic Rats

Diabetic retinopathy(DR)is a common cause of blindness all over the world.Bone marrow mesenchymal stem cells(BMSCs)have been considered as a promising strategy for retinal regeneration in the treatment of DR.However,the poor viability and low levels of BMSCs engraftment limit the therapeutic potential of BMSCs.The present study aimed to examine the direct induction of BMSCs differentiation into the cell types related to retinal regeneration by using soluble cytokine ciliary neurotrophic factor(CNTF).We observed remarkably increased expression of cellular retinaldehyde-binding protein(CRALBP)and retinoid isomerohydrolase(RPE65)in BMSCs treated with CNTF in vitro,indicating the directional differentiation of BMSCs into the retinal pigment epithelium(RPE)cells,which are crucial for retinal healing.In vivo,the diabetic rat model was established by use of streptozotocin(STZ),and animals treated with BMSCs+CNTF exhibited better viability and higher delivery efficiency of the transplanted cells than those treated with BMSCs injection alone.Similar to the in-vitro result,treatment with BMSCs and CNTF combined led to the differentiation of BMSCs into beneficial cells(RPE cells),and accelerated retinal healing characterized by the activation of rod photoreceptor cells and phagocytosis function of RPE cells.In conclusion,CNTF contributes to the differentiation of BMSCs into RPE cells,which may help overcome the current stem cell therapy limitations in the field of retinal regeneration.

Role of cytokine receptor-like factor 1 in hepatic stellate cells and fibrosis

AIM: To elucidate the role of cytokine receptor-like factor 1 (CRLF1) in hepatic stellate cells and liver fibrosis.

Effects of Jinmaitong Capsule(筋脉通胶囊) on Ciliary Neurotrophic Factor in Sciatic Nerves of Diabetes Mellitus Rats

ABSTRACT Objective： To study the effects of the Chinese medicine Jinmaitong Capsule （筋脉通胶囊, JMT） on the pathomorphology of sciatic nerves, ciliary neurotrophic factor （CNTF）, and the mRNA expressions of CNTF in rats with streptozotocin-induced diabetes mellitus （STZ-DM）. Methods： The animal model was established by one time intraperitoneal injection of streptozotocin. The rats were simply divided by random into 5 groups including model group, low-dose JMT group （JL）, medium-dose JMT group （JM）, high-dose JMT group （JH） and neurotropin group. For each of the above 5 groups, a group of 10 normal Wistar rats matched in body weight, age and gender were set as normal group. Intragastric administrations were started after the animal model established. The JL group were administered with five times the JMT dose recommended for a human adult; the JM group were administered with ten times the JMT dose recommended for a human adult; the JH group were administered with twenty times the JMT dose recommended for a human adult. The neurotropin group was administered with ten times the neurotropin dose recommended for a human adult. All rats were given intragastric administration for 16 weeks and then killed. In the 4th, 8th, 12th, 16th week, body weight and blood glucose level were detected before and after the intervention. The morphologic changes of the sciatic nerves were observed by optical microscope and transmission electron microscope. The CNTF- mRNA expressions were detected by real-time fluorescent quantitative polymerase chain protein, and the CNTF protein expressions were detected by immunohistochemical method. Results： The blood glucose levels of the STZ-DM rats were much higher than normal group （P〈0.01）, and there was no apparent difference between any treatment groups and the model group （P〉0,05）. Before and after the intervention in the 4th, 8th, 12th, 16th week, there were no significant differences in the body weight among all the groups （P〉0.05）. The sciatic nerves of STZ-DM rats might have pathomorphological changes in axons, myelin sheaths, and interstitium. The levels of CNTF and CNTF-mRNA expressions in the STZ-DM rats were both significantly decreased （P〈0.01）. The sciatic nerves of STZ-DM rats might have pathomorphological changes in axons, myelin sheaths, and interstitium. Conclusion： JMT could improve the pathomorphology of sciatic nerves by increasing CNTF＇s and CNTF-mRNA expressions in sciatic nerve tissues, and promote the repair and regeneration of damaged nerve fibers.

Expression of ciliary neurotrophic factor after induction of ocular hypertension in the retina of rats

Background Glaucoma is mainly characterized by the loss of retinal ganglion cells. Ciliary neurotrophic factor （CNTF） is believed to stimulate the regeneration of axons of retinal ganglion cells, The objective of our study was to detect the expression of CNTF in the retina of a rat glaucoma model with increased intraocular pressure （IOP）,Methods The rat glaucoma model was set up by electrocoagulating at least three episcleral and limbal veins, The location and the expression level of CNTF were detected at 1, 3, 7, 14, and 28 days post-surgery by immunohistochemistry, semiquantitative reverse-transcription polymerase chain reaction （RT-PCR）, and Western blot analysis.Results The rat glaucoma model with chronic, moderately elevated IOP was successfully produced, A minimum expression of CNTF was found in the ganglion cell layer of the retinas of the control group, and temporally increased expression and intensity of CNTF were found in the experimental retinas. Conclusion The expression of endogenous CNTF in the rat retina was found altered after the induction of ocular hypertension.

Effect of ciliary neurotrophic factor on the reactive astro-gliosis of cultured astrocytes from newborn rat brain

The effect of ciliary neurotrophic factor (CNTF) on reactive astrogliosis was studied on a mechanical scratch model of the confluent astrocytic cultures from newborn rat brain. Following injury, the astrocytes at the edge of the injured area displayed a typical process of the reactive astrogliosis. This process included apparently hyperplastic change and significantly increased GFAP expression of the flat astrocytes, and migration to the injured area of the O-2A progenitor cells and their differentiation into process-bearing astrocytes. Exogenous CNTF applied to the cell cultures significantly promoted the hyperplasia and GFAP expression of the flat astrocytes. The results suggest that CNTF can enhance the reactive astrogliosis in the injured area.

Expression and cloning of ciliary neurotrophic factor gene from human optic glioma and glioblastoma cell line

Ciliary neurotrophic factor (CNTF) is the first neurokine to be found out for the potency to promote motoneuron survival in vitro and in vivo, and it does play a role in the development and regeneration of the nervous system. CNTF has been found up mainly in the astrocyte and Schwann cell. Its gene is located in the proximal part of long arm of chromosome 11, and apparently heterogenous to the gene of neurotrophins, there is

新型纳米睫状神经营养因子复合物玻璃体腔注射对食蟹猴眼部的安全性——形态学评价

目的评估一种新型纳米神经营养因子复合物(NP-CNTFs)在非人灵长类动物眼内应用的安全性。方法利用纳米工艺制备包裹睫状神经营养因子(CNTF)的纳米粒。选取3只成年雄性食蟹猴,单眼玻璃体腔注射10μl NP-CNTFs(1μg/μl)作为NP-CNTFs组,对侧眼注射等体积磷酸盐缓冲液作为对照组。在注射前、注射后第3天和第7天,对食蟹猴行常规眼前节检查以评估结膜充血、前房闪辉及前房细胞等眼部症状并评分;采用彩色眼底照相观察眼底情况;采用频域光学相干断层扫描(SD-OCT)检测视网膜形态结构及厚度。结果所制备NP-CNTFs粒径为(317±3)nm,多分散性指数为0.042±0.015,Zeta电位为(-38.9±0.7)mV,具备较好的稳定性、生物利用度和生物相容性。眼前节检查显示,NP-CNTFs组在注射后第3天表现出较对照组稍明显的结膜充血、前房闪辉和前房细胞,但在注射后第7天基本恢复正常。NP-CNTFs组与对照组注射后第3天眼前节症状评分分别为(2.67±0.88)和(1.00±0.58)分,注射后第7天分别为(0.67±0.33)和(0.33±0.33)分,组间比较差异均无统计学意义(t=2.50、1.00,均P>0.05)。彩色眼底照相结果显示,NP-CNTFs组和对照组在注射后第7天眼底均正常,未见玻璃体混浊、玻璃体出血、视网膜出血或视盘水肿等异常改变。SD-OCT结果显示,NP-CNTFs组和对照组在注射后第7天均未见明显视网膜组织学改变。NP-CNTFs组和对照组视网膜神经纤维层厚度分别为(107.67±0.88)和(111.00±3.22)μm,黄斑中央凹厚度分别为(255.67±2.03)和(254.67±3.84)μm,组间比较差异均无统计学意义(t=1.43、0.50,均P>0.05)。结论新型纳米药物NP-CTNFs在食蟹猴眼内应用的安全性较好。

鲁拉西酮联合草酸艾司西酞普兰治疗老年卒中后抑郁的疗效观察

目的观察鲁拉西酮联合草酸艾司西酞普兰治疗老年卒中后抑郁的疗效。方法回顾性选取2020年5月至2021年6月温州市第七人民医院收治的92例老年卒中后抑郁患者为研究对象,采用鲁拉西酮联合草酸艾司西酞普兰治疗46例,为观察组;仅草酸艾司西酞普兰治疗46例,为对照组。观察并比较两组患者疗效、治疗期间不良反应以及治疗前与治疗6个月后事件相关电位参数[包括失匹配负波(MMN)和P300的潜伏期及波幅]、实验室指标[包括血清尿酸(UA)、睫状神经营养因子(CNTF)、脑源性神经营养因子(BDNF)水平]、神经功能[采用美国国立卫生研究院卒中量表(NIHSS)评价]、抑郁状况[采用17项汉密尔顿抑郁量表(HAMD-17)评价]等。结果观察组临床总有效率明显高于对照组(93.48%比78.26%,P=0.036)。治疗后,两组患者MMN潜伏期、P300潜伏期均明显缩短(均P<0.05),MMN波幅、P300波幅均明显增加(均P<0.05),血清UA、CNTF、BDNF水平均明显升高(均P<0.05),NIHSS、HAMD-17评分均明显降低(均P<0.05);且观察组上述指标较对照组变化均更明显(均P<0.05)。两组患者合计不良反应发生率比较,差异无统计学意义(10.87%比8.70%,P=0.726)。结论鲁拉西酮联合草酸艾司西酞普兰治疗老年卒中后抑郁的疗效较好,能改善事件相关电位、神经功能缺损以及抑郁状况,提高血清UA、CNTF、BDNF水平,且安全性较高。

神经营养因子影响视神经夹伤后视网膜GAP-43mRNA表达变化

目的:观察大鼠视神经夹伤后视网膜上GAP-43基因的变化,观察玻璃体腔内注射睫状神经营养因子(ciliarnyeurotrophicfacto,rCNTF)和腺病毒介导脑源性神经营养因子(adenovirallydeliveredbrain-dreivedneurotrophicfacto,rAd-BDNF)对视网膜上GAP-43mRNA的影响。方法:成年SD大鼠球后2mm处作视神经夹伤模型,经巩膜玻璃体腔内注射微量神经营养因子(neurotraphicfactor,sNFs),应用原位杂交法观察视网膜的GAP-43mRNA的变化。结果:正常SD大鼠视网膜上仅在节细胞层检测到少数细胞存在GAP-43mRNA杂交信号,对照组和CNTF治疗组视神经夹伤后1wk内可观察到视网膜神经节层中存在较强的GAP-43mRNA杂交信号,伤后2wk时已减弱至伤前,Ad-BDNF治疗组在视神经夹伤后4wk内在视网膜上均能观察到GAP-43mRNA的杂交信号,其中在夹伤后1～2wk时杂交信号相对较强。结论:视神经夹伤能上调视网膜上GAP-43mRNA表达,玻璃体腔内注射Ad-BDNF在伤后4wk内均能上调视网膜上GAP-43mRNA表达。

视神经损伤后视网膜CNTF及CNTFRα免疫组织化学检测

目的研究视神经损伤后睫状神经营养因子(ciliaryneurotrophicfactor,CNTF)及其受体(ciliaryneurotrophicfactorrecepterα,CNTFRα)在大鼠视网膜中的定位表达变化。方法采用钳夹法制作大鼠视神经损伤模型。分别于伤后1d、3d、7d、14d、28d取眼球,以正常大鼠视网膜为对照,运用免疫组织化学方法检测视神经损伤后CNTF和CNTFRα的表达变化。结果在正常对照组中,由视锥视杆细胞外节组成的视网膜视锥视杆细胞层均有大量的CNTF及CNTFRα存在,在其它各层也存在散在颗粒状分布的CNTF及CNTFRα。视神经损伤后,CNTF及CNTFRα在视网膜各层显著增加,并呈弥漫性分布,在损伤后3d、7d、14d与正常对照组比较相差非常显著(P<0.01)。损伤后7d,CNTF及CNTFRα在视网膜各层表达达高峰,在损伤后28d2者的表达均显著高于正常对照组(CNTF:P=0.02<0.05;CNTFR:P=0.015<0.05)。结论视神经不全损伤导致了视网膜CNTF和CNTFRα表达量的增加和分布的改变,可能是视网膜神经元损伤后自我保护的一种反应。

睫状神经营养因子对脊髓神经元的保护作用

目的 :研究脊髓损伤后脊髓神经元内酶学的变化 ,并探索睫状神经营养因子 (CNTF)对神经元的保护作用。 方法 :用 Allen改良法打击模型致 SD大鼠 T8脊髓损伤 ,分别于术前及术后 3,7,10 d测定脊髓组织内乙酰胆碱酯酶 (ACh E)和酸性磷酸酶 (ACP)的含量。结果 :ACh E于术后持续下降 ;ACP在术后第 3天开始上升 ,第 7天升至最高 ,以后逐渐下降 ;用 CNTF处理的大鼠上述两种酶变化的幅度较小 ,且整个过程也比较平稳。 结论