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Beta-nerve growth factor promotes neurogenesis and angiogenesis during the repair of bone defects 被引量:9
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作者 Wei-hui Chen Chuan-qing Mao +1 位作者 Li-li Zhuo Joo L.Ong 《Neural Regeneration Research》 SCIE CAS CSCD 2015年第7期1159-1165,共7页
We previously showed that the repair of bone defects is regulated by neural and vascular signals. In the present study, we examined the effect of topically applied β-nerve growth factor(β-NGF) on neurogenesis and ... We previously showed that the repair of bone defects is regulated by neural and vascular signals. In the present study, we examined the effect of topically applied β-nerve growth factor(β-NGF) on neurogenesis and angiogenesis in critical-sized bone defects filled with collagen bone substitute. We created two symmetrical defects, 2.5 mm in diameter, on either side of the parietal bone of the skull, and filled them with bone substitute. Subcutaneously implanted osmotic pumps were used to infuse 10 μgβ-NGF in PBS(β-NGF + PBS) into the right-hand side defect, and PBS into the left(control) defect, over the 7 days following surgery. Immunohistochemical staining and hematoxylin-eosin staining were carried out at 3, 7, 14, 21 and 28 days postoperatively. On day 7, expression of β III-tubulin was lower on the β-NGF + PBS side than on the control side, and that of neurofilament 160 was greater. On day 14, β III-tubulin and protein gene product 9.5 were greater on the β-NGF + PBS side than on the control side. Vascular endothelial growth factor expression was greater on the experimental side than the control side at 7 days, and vascular endothelial growth factor receptor 2 expression was elevated on days 14 and 21, but lower than control levels on day 28. However, no difference in the number of blood vessels was observed between sides. Our results indicate that topical application of β-NGF promoted neurogenesis, and may modulate angiogenesis by promoting nerve regeneration in collagen bone substitute-filled defects. 展开更多
关键词 nerve regeneration β-nerve growth factor collagen angiogenesis protein gene product 9.5 vascular endothelial growth factor β III-tubulin neural regeneration
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Adenovirus-mediated human β-nerve growth factor gene transfer has a protective effect on cochlear spiral ganglion after blast exposure 被引量:2
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作者 吴建 刘冰 +2 位作者 何金 范静平 孙爱华 《Journal of Medical Colleges of PLA(China)》 CAS 2007年第5期293-297,共5页
Objective:To study whether adenovirus-mediated human β-nerve growth factor (Ad-hNGFβ) gene has any protective effect on blast hearing impairment. Methods:Deafness was induced by blast exposure (172.0 dB) in 30 healt... Objective:To study whether adenovirus-mediated human β-nerve growth factor (Ad-hNGFβ) gene has any protective effect on blast hearing impairment. Methods:Deafness was induced by blast exposure (172.0 dB) in 30 healthy guinea pigs. On day 7 of blast exposure, Ad-hNGFβ was infused into the perilymphatic space of 20 animals as the study group (hNGFβ group), and artificial perilymph fluid (APF) was infused into the perilymphatic space of the other 10 animals as the control group. At weeks 1, 4 and 8 after blast exposure, the animals were sacrificed and the cochleae were removed for immunohistochemical and HE stainings. Results: Expression of Ad-hNGFβ protein was detected in each turn of the cochlea at the 1st week, with almost equal intensity in all turns. At the 4th week, the reactive intensity of the expression of Ad-hNGFβ protein decreased. At the 8th week, no expression was detectable. The results of HE staining showed that the amount of spiral ganglions in hNGFβ group was significantly greater than that of the control group at week 4 (P<0.01). Conclusion: Ad-hNGFβ can be expressed at a high level and for a relatively long period in the blast impaired cochlea, suggesting that Ad-hNGFβ has a protective effect on cochlear spiral ganglion cells after blast exposure and the efficient gene transfer into cochlea had been achieved without toxicity. 展开更多
关键词 recombinant adenovirus nerve growth factor blast exposure hearing loss spiral ganglion gene therapy
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Beta-nerve growth factor gene therapy alleviates pyridoxine-induced neuropathic damage by increasing doublecortin and tyrosine kinase A in the dorsal root ganglion 被引量:2
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作者 Hyun-Kee Cho Woosuk Kim +4 位作者 Kwon-Young Lee Jin-Ok Ahn Jung Hoon Choi In Koo Hwang Jin-Young Chung 《Neural Regeneration Research》 SCIE CAS CSCD 2020年第1期162-168,共7页
Beta-nerve growth factor(β-NGF) is known to be a major leading cause of neuronal plasticity. To identify the possible action mechanisms of β-NGF gene therapy for sciatic nerve recovery, experimental dogs were random... Beta-nerve growth factor(β-NGF) is known to be a major leading cause of neuronal plasticity. To identify the possible action mechanisms of β-NGF gene therapy for sciatic nerve recovery, experimental dogs were randomly divided into control, pyridoxine, and pyridoxine + β-NGF groups. We observed chronological changes of morphology in the dorsal root ganglia in response to pyridoxine toxicity based on cresyl violet staining. The number of large neurons positive for cresyl violet was dramatically decreased after pyridoxine intoxication for 7 days in the dorsal root ganglia and the neuron number was gradually increased after pyridoxine withdrawal. In addition, we also investigated the effects of β-NGF gene therapy on neuronal plasticity in pyridoxine-induced neuropathic dogs. To accomplish this, tyrosine kinase receptor A(TrkA), βIII-tubulin and doublecortin(DCX) immunohistochemical staining was performed at 3 days after the last pyridoxine treatment. TrkA-immunoreactive neurons were dramatically decreased in the pyridoxine group compared to the control group, but strong TrkA immunoreactivity was observed in the small-sized dorsal root ganglia in this group. TrkA immunoreactivity in the dorsal root ganglia was similar between β-NGF and control groups. The numbers of βIII-tubulin-and DCX-immunoreactive cells decreased significantly in the pyridoxine group compared to the control group. However, the reduction of βIII-tubulin-and DCX-immunoreactive cells in the dorsal root ganglia in the β-NGF group was significantly ameliorated than that in the pyridoxine group. These results indicate that β-NGF gene therapy is a powerful treatment of pyridoxine-induced neuropathic damage by increasing the TrkA and DCX levels in the dorsal root ganglia. The experimental protocol was approved by the Institutional Animal Care and Use Committee(IACUC) of Seoul National University, South Korea(approval No. SNU-060623-1, SNU-091009-1) on June 23, 2006 and October 9, 2009, respectively. 展开更多
关键词 β-nerve growth factor βIII-tubulin DOUBLECORTIN gene therapy neuron-glial antigen 2 neuropathy PYRIDOXINE
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Role of Nerve Growth Factor (NGF) and Its Receptor Tyrosine Kinase A (TrK A) in Egyptian Cirrhotic Patients with Pruritus
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作者 Amr Zaghloul Hanan Assaf +4 位作者 Reham Ezz Mohamed Malak Mahmoud Rezk Ashraf Askar Essam El-dinNada 《Open Journal of Gastroenterology》 2018年第9期317-326,共10页
Background: Pruritus is a distressing symptom of cholestatic, inflammatory, and malignant liver diseases. It is a common symptom in many biliary and cholestatic disorders such as primary biliary cirrhosis (PBC). Sever... Background: Pruritus is a distressing symptom of cholestatic, inflammatory, and malignant liver diseases. It is a common symptom in many biliary and cholestatic disorders such as primary biliary cirrhosis (PBC). Several mechanisms are generally accepted as possible explanations to the underlying basis of itch. However, the exact pathophysiology of pruritus in liver diseases remains unclear. The cutaneous and central neurobiology of pruritus is complex and underlies a regulation of variable mechanisms. At present, not all mechanisms including neuromediators and receptors are known. Objective: Our objective is to evaluate whether the expression pattern of NGF and its receptor TrK A has a role in pruritus in a group of Egyptian cirrhotic patients. Patients and Methods: Forty Patients with liver cirrhosis were enrolled in the study depending on clinical evidence of stigmata of chronic liver disease (e.g. jaundice, ascites, palmar erythema, spider naevi, etc.) and ultrasonographic features of liver cirrhosis (e.g. coarse echo texture, shrunken liver, etc.). Patients were divided into two groups. Group (1): included 20 patients cirrhotic patients without pruritus. Group (2): included 20 patients cirrhotic patients with pruritus. A group of age and sex matched healthy twenty volunteers as a control. Results: After evaluation of histopathological using hematoxylin and eosin stained sections (H&E) was done. There was positive correlation between NGF protein expression and severity of pruritus in cirrhotic patients with pruritus (r = 0.876, p value ≤ 0.001). Also there was positive correlation between TrK A protein expression and severity of pruritus in cirrhotic patients with pruritus (r = 0.44, p value ≤ 0.05). Conclusions: We report, for the first time, role of these proteins (NGF/TrK A) in the mechanism of pruritus in cirrhotic patients and may provide a potential target for new treatment of pruritus in cirrhotic. 展开更多
关键词 Liver Cirrhosis ITCHING nerve growth factor (ngf) and ITS RECEPTOR Tyrosine Kinase A (TrK A)
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Effect of calcitonin gene-related peptide and nerve growth factor on spatial learning and memory abilities of rats following focal cerebral ischemia/reperfusion
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作者 Guangshun Zheng1, Yongjie Yang2, Xiubin Fang3 1Department of Neurosurgery, Second Hospital of Xiamen, Xiamen 361021, Fujian Province, China 2Department of Neurosurgery, Second Hospital Affiliated to China Medical University, Shenyang 110004, Liaoning Province, China 3Department of Neurobiology, Basic Medical College of China Medical University, Shenyang 110001, Liaoning Province, China 《Neural Regeneration Research》 SCIE CAS CSCD 2006年第8期673-676,共4页
BACKGROUND: Calcitonin gene-related peptide (CGRP) and nerve growth actor (NGF) cam improve spatial learning and memory abilities of rats with cerebral ischemia/reperfusion; however, the effect of combination of them ... BACKGROUND: Calcitonin gene-related peptide (CGRP) and nerve growth actor (NGF) cam improve spatial learning and memory abilities of rats with cerebral ischemia/reperfusion; however, the effect of combination of them on relieving learning and memory injury following cerebral ischemia/reperfusion should be further studied. OBJECTIVE: To study the effects of exogenous CGRP and NGF on learning and memory abilities of rats with focal cerebral ischemia/reperfusion. DESIGN: Randomized controlled animal study. SETTING: Department of Neurosurgery, the Second Hospital of Xiamen; Department of Neurosurgery, the Second Affiliated Hospital of China Medical University; Department of Neurobiology, Basic Medical College of China Medical University. MATERIALS: A total of 30 healthy male SD rats, aged 8 weeks, of clean grade, weighing 250-300 g, were provided by Experimental Animal Department of China Medical University. All rats were randomly divided into sham-operation group, ischemia/reperfusion group and treatment group with 10 in each group. The main reagents were detailed as the follows: 100 g/L chloral hydrate, 0.5 mL CGRP (2 mg/L, Sigma Company, USA), and NGF (1× 106 U/L, 0.5 mL, Siweite Company, Dalian). METHODS: The experiment was carried out in the Department of Neurobiology, Basic Medical College of China Medical University from February to July 2005. Rat models of middle cerebral artery occlusion were established by method of occlusion, 2 hours after that rats were anesthetized and the thread was slightly drawn out for 10 mm under direct staring to perform reperfusion. Rats in the ischemia/reperfusion group received intraperitoneal injection of 1 mL saline via the abdomen at two hours later, while rats in the treatment group at 2 hours later received intraperitoneal injection of 2 mg/L CGRP (0.5 mL) and 1×106 U/L NGF (0.5 mL) once a day for 10 successive days. First administration was accomplished within 15 minutes after ischemia/reperfusion. Rats in the sham-operation group were separated of the vessels without occlusion or administration. The neural function was evaluated with Zea Longa 5-grade scale. Animals with the score of one, two and three points received Morris water-maze test to measure searching time on platform (omitting platform-escaping latency). Meanwhile, leaning and memory abilities of animals were reflected through testing times of passing through platform per minute. MAIN OUTCOME MEASURES: Experimental results of omitting platform-escaping latency and spatial probe. RESULTS: Three and two rats in the ischemia/reperfusion group and treatment group respectively were not in accordance with the criteria in the process, and the rest were involved in the final analysis. ① Comparisons of platform-escaping latency during Morris water-maze test in all the three groups: Ten days after modeling, the platform-escaping latency in the ischemia/reperfusion group was obviously longer than that in sham-operation group (P < 0.01), and was significantly shorter than that in the treatment group (P < 0.01). ② Comparisons of times of passing through platform in all the three groups: Times of passing through platform were remarkably less in the ischemia/reperfusion group than those in the sham-operation group [(1.79±0.39), (4.30±0.73) times/minute, P < 0.01], and those were markedly more in the treatment group than the ischemia/reperfusion group [(3.16±1.03), (1.79±0.39) times/minute, P < 0.01]. CONCLUSION: CGRP and NGF are capable of ameliorating the abilities of spatial learning and memory in MCAO rats, which indicates that CGRP and NGF can protect ischemic neurons. 展开更多
关键词 Effect of calcitonin gene-related peptide and nerve growth factor on spatial learning and memory abilities of rats following focal cerebral ischemia/reperfusion CGRP MCAO gene
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A study on peripheral nerve regeneration via biomimetic conduits loadedwith Schwann cells and nerve growth factor
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《Chinese Journal of Biomedical Engineering(English Edition)》 2001年第2期53-55,共3页
关键词 ngf A study on peripheral nerve regeneration via biomimetic conduits loadedwith Schwann cells and nerve growth factor SC
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Uncoupling neurotrophic function from nociception of nerve growth factor: what can be learned from a rare human disease? 被引量:5
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作者 Kijung Sung Wanlin Yang Chengbiao Wu 《Neural Regeneration Research》 SCIE CAS CSCD 2019年第4期570-573,共4页
Nerve growth factor(NGF) is a powerful trophic factor that provides essential support for the survival and differentiation of sympathetic and sensory neurons during development. However, NGF also activates nociceptors... Nerve growth factor(NGF) is a powerful trophic factor that provides essential support for the survival and differentiation of sympathetic and sensory neurons during development. However, NGF also activates nociceptors contributing significantly to inflammatory pain and neuropathic pain after tissue injury. As such anti-NGF based therapies represent a promising strategy for pain management. Because of dose-dependent serious side effects such as back pain, injection site hyperalgesia, clinical trials of using NGF to treat various disorders such as diabetic neuropathies, chemotherapy-induced and human immunodeficiency virus-associated peripheral neuropathies were all discontinued. Thus far, worldwide clinical applications of NGF in treating patients are very limited except in China. Hereditary sensory autonomic neuropathy type V(HSAN V) is an extremely rare disease. Genetic analyses have revealed that HSAN V is associated with autosomal recessive mutations in NGF. One of the mutations occurred at the 100^(th) position of mature NGF resulting in a change of residue from arginine to tryptophan(R100W). Although those HSAN V patients associated with the NGF^(R100W) mutation suffer from severe loss of deep pain, bone fractures and joint destruction, interestingly patients with the NGF^(R100W) mutation do not show apparent cognitive deficits, suggesting important trophic support function is preserved. We believe that NGF^(R100W) provides an ideal tool to uncouple the two important functions of NGF: trophic versus nociceptive. Studies from investigators including ourselves have indeed confirmed in animal testing that the NGF^(R100W) no longer induced pain. More importantly, the trophic function seemed to be largely preserved in NGF harboring the R100W mutation. On the mechanistic level, we found that the NGF^(R100W) mutation was capable of binding to and signaling through the tyrosine receptor kinase A receptor. But its ability to bind to and activate the 75 kDa neurotrophic factor was significantly diminished. The significance of these findings is at least two folds: 1) the NGF^(R100W) mutation can be used as an alternative to the wildtype NGF to treat human conditions without eliciting pain; and 2) the 75 kDa neurotrophic factor may serve as a novel target for pain management. We will discuss all the details in this mini-review. 展开更多
关键词 hereditary sensory and autonomic neuropathy V nerve growth factor ngfR100W mutation pain tyrosine RECEPTOR kinase A p75 NEUROTROPHIC factor RECEPTOR
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Nerve Growth Factor Enhances Tau Isoform Expression and Transcription in IMR32 Cells 被引量:2
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作者 Cheryl L. Cragg Bettina E. Kalisch 《Neuroscience & Medicine》 2014年第2期119-130,共12页
The present study characterized the nerve growth factor (NGF)-mediated regulation of tau protein expression and transcription in IMR32 human neuroblastoma cells. Treatment of IMR32 cells with 50 ng/mL NGF resulted in ... The present study characterized the nerve growth factor (NGF)-mediated regulation of tau protein expression and transcription in IMR32 human neuroblastoma cells. Treatment of IMR32 cells with 50 ng/mL NGF resulted in increased levels of specific tau protein isoforms. A 550 bp fragment of the tau promoter was cloned and treatment of transfected IMR32 and PC12 cells with NGF also resulted in increased promoter activation, suggesting that the NGF-mediated increase in tau isoforms is regulated, at least in part, at the level of transcription. Pretreatment with the MAP kinase inhibitor U0126 or the PKC inhibitor bisindolylmaleimide 1 (BIS-1) attenuated the NGF-mediated increase in tau transcription, indicating that the NGF-mediated activation of the MAP kinase and PKC signaling pathways modulate tau transcription. Pre-treatment of cells with the Akt inhibitor, LY294002 or with NOS inhibitors Nω-nitro-L-arginine methylester (L-NAME) or s-methylisothiourea (S-MIU) had no effect on the NGF-mediated increase in tau promoter activation, suggesting that NO and the NGF-Akt signaling pathway do not modulate tau transcription. Taken together, these data demonstrate that NGF increases the levels of multiple human tau isoforms in IMR32 cells which may result, at least in part, from NGF-mediated PKC and MAP kinase-induced tau transcription. 展开更多
关键词 nerve growth factor (ngf) TAU Signal TRANSDUCTION Transcription NITRIC Oxide (NO) IMR32 CELLS PC12 CELLS
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Nerve growth factor downregulates c-jun mRNA and Caspase-3 in striate cortex of rats after transient global cerebral ischemia/reperfusion 被引量:1
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作者 Dacheng Jin Tiemin Wang Xiubin Fang 《Neural Regeneration Research》 SCIE CAS CSCD 2006年第4期289-292,共4页
BACKGROUND: Immediate early gene (lEG) c-jun is a sensitive marker for functional status of nerve cells. Caspase-3 is a cysteine protease, which is a critical regulator of apoptosis. The effect of exogenous nerve g... BACKGROUND: Immediate early gene (lEG) c-jun is a sensitive marker for functional status of nerve cells. Caspase-3 is a cysteine protease, which is a critical regulator of apoptosis. The effect of exogenous nerve growth factor (NGF) on the expression of c-jun mRNA and Caspase-3 protein in striate cortex of rats with transient global cerebral ischemia/reperfusion (IR) is unclear. OBJECTIVE: To study the protective effect of exogenous NGF on the brain of rats with transient globa cerebral IR and its effecting pathway by observing the expression of c-jun mRNA and Caspase-3 protein. DESIGN: Randomized controlled animal trial SETTING: Department of Neural Anatomy, Institute of Brain, China Medical University MATERIALS:Eighteen healthy male SD rats of clean grade, aged 1 to 3 months, with body mass of 250 to 300 g, were involved in this study. NGF was provided by Dalian Svate Pharmaceutical Co.,Ltd. c-jun in situ hybridization detection kit, Caspase-3 antibody and SABC kit were purchased from Boster Biotechnology Co.. Ltd. METHODS: This trial was carried out in the Department of Neural Anatomy, Institute of Brain, China Medical University during September 2003 to April 2005. (1) Experimental animals were randomized into three groups with 6 in each: sham-operation group, IR group and NGF group.(2)After the rats were anesthetized, the bilateral common carotid arteries and right external carotid arteries of rats were bluntly dissected and bilateral common carotid arteries were clamped for 30 minutes with bulldog clamps. Reperfusion began after buldog clamps were removed. Normal saline of lmL and NGF (1×10^6 U/L) of 1 mL was injected into the common carotid artery of rats via right external carotid arteries in the IR group and NGF group respectively. The injection was conducted within 30 minutes, and then the right external carotid arteries were ligated. In the sham-operation group, occlusion of bilateral common carotid arteries and administration of drugs were omitted.GAll the rats were executed by decollation at 3 hours after modeling. The animals were fixed with phosphate buffer solution (PBS, 0.1 mol/L) containing 40 g/L polyformaldehyde, their brains were quickly removed. The coronal section tissue mass containing striate cortex about 3 mm before line between two ears was taken and made into successive frozen sections.(4)The expression of c-jun mRNA and Caspase-3 protein in striate cortex of global cerebral ischemia rats were detected with in situ hybridization, immunohistochemistry and microscope image analysis. (5)t test was used for comparing the difference of the measurement data. MAIN OUTCOME MEASURES:Comparison of the expression of lEG c-jun mRNA and Caspase-3 protein in striate cortex of brain of rats in each group. RESULTS:All the 18 SD rats were involved in the analysis of results. The c-jun mRNA and Caspase-3 protein positive reaction cells were found brown yellow in the striate cortex of rats, and most of them were in lamellas Ⅱ and Ⅲ, mainly presenting round or oval. The expression of c-jun mRNA and Caspase-3 protein in sham-operation group was weak or negative. The average gray value of c-jun mRNA and Caspase-3 protein in the IR group was significantly lower than that in the sham-operation group (49.52±4.13 vs. 95.48± 5.28; 74.73±4.29 vs. 162.38±9.16,P 〈 0.01). The average gray value of c-jun mRNA and Caspase-3 protein in the NGF group was significantly higher than that in the IR group (63.96±4.25 vs.49.52±4.13; 83.98± 4.13 vs. 74.73±4.29, P〈 0.05). CONCLUSION: NGF can protect ischemic neurons by down-regulating the expression of c-jun mRNA and Caspase-3 protein in striate cortex of global cerebral ischemia rats. 展开更多
关键词 MRNA nerve growth factor downregulates c-jun mRNA and Caspase-3 in striate cortex of rats after transient global cerebral ischemia/reperfusion ngf
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Maternal Lead Exposure Induces Down-regulation of Hippocampal Insulin-degrading Enzyme and Nerve Growth Factor Expression in Mouse Pups
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作者 LI Xing LI Ning +6 位作者 SUN Hua Lei YIN Jun TAO Yu Chang MAO Zhen Xing YU Zeng Li LI Wen Jie John D BOGDEN 《Biomedical and Environmental Sciences》 SCIE CAS CSCD 2017年第3期215-219,共5页
Lead exposure is a known potential risk factor for neurodegenerative diseases such as Alzheimer’s disease (AD). Exposure to lead during the critical phase of brain development has been linked with mental retardatio... Lead exposure is a known potential risk factor for neurodegenerative diseases such as Alzheimer’s disease (AD). Exposure to lead during the critical phase of brain development has been linked with mental retardation and hypophrenia in later life. 展开更多
关键词 AD Maternal Lead Exposure Induces Down-regulation of Hippocampal Insulin-degrading Enzyme and nerve growth factor Expression in Mouse Pups IDE ngf
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姜黄素对TGF-β1诱导的心脏成纤维细胞表达NGF、IL-1β、TNF-α的影响及机制研究 被引量:1
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作者 刘玉旋 王新慧 +4 位作者 杨阳 马鑫 白芳芳 姬新珂 李平 《新疆医科大学学报》 CAS 2024年第6期772-777,784,共7页
目的观察姜黄素对转化生长因子-β1(Transforming growth factor-β1,TGF-β1)诱导的心脏成纤维细胞表达神经生长因子(Nerve growth factor,NGF)和炎症因子的影响,并探讨其可能的作用机制。方法在体外通过TGF-β1刺激心脏成纤维细胞,模... 目的观察姜黄素对转化生长因子-β1(Transforming growth factor-β1,TGF-β1)诱导的心脏成纤维细胞表达神经生长因子(Nerve growth factor,NGF)和炎症因子的影响,并探讨其可能的作用机制。方法在体外通过TGF-β1刺激心脏成纤维细胞,模拟心肌梗死(Myocardial in-farction,MI)模型。分组为Control组、TGF-β1组、美托洛尔(Myto)组,姜黄素微、低、中、高剂量(CCM-5、10、20、40)组。造模时间为48 h,药物处理时间为48 h。使用RT-qPCR检测NGF、Hes1、Hey1、NICD的mRNA表达水平,Western blot法检测NGF、Hes1、Hey1、NICD的蛋白表达水平,Elisa检测细胞上清中炎症因子IL-1β、TNF-α含量。结果与Control组比较,TGF-β1组细胞中NGF、Hes1、Hey1、NICD的mRNA及其蛋白表达水平明显升高(P<0.05),细胞上清中IL-1β、TNF-α含量明显升高(P<0.05)。与TGF-β1组比较,CCM-5组、CCM-10组、CCM-20组、CCM-40组的NGF、Hes1、Hey1、NICD的mRNA及蛋白表达水平与IL-1β、TNF-α含量均有不同程度的降低,部分组间比较差异有统计学意义(P<0.05),并且这些指标具有姜黄素浓度依赖性。结论姜黄素可以下调TGF-β1诱导的心脏成纤维细胞中NGF和IL-1β、TNF-α的表达,具有抗交感神经重构和抗炎作用,其机制可能与Notch信号通路的活化有关。 展开更多
关键词 姜黄素 心脏成纤维细胞 NOTCH信号通路 神经生长因子 交感神经重构
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Angiogenesis and nerve regeneration induced by local administration of plasmid pBud-coVEGF165-coFGF2 into the intact rat sciatic nerve 被引量:5
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作者 Ruslan Masgutov Alina Zeinalova +11 位作者 Alexey Bogov Galina Masgutova Ilnur Salafutdinov Ekaterina Garanina Valeriia Syromiatnikova Kamilla Idrisova Adelya Mullakhmetova Dina Andreeva Liliya Mukhametova Adilet Kadyrov Igor Pankov Albert Rizvanov 《Neural Regeneration Research》 SCIE CAS CSCD 2021年第9期1882-1889,共8页
Vascular endothelial growth factor(VEGF) and fibroblast growth factor 2(FGF2) are well-known growth factors involved in the regeneration of various tissues and organs, including peripheral nerve system. In the present... Vascular endothelial growth factor(VEGF) and fibroblast growth factor 2(FGF2) are well-known growth factors involved in the regeneration of various tissues and organs, including peripheral nerve system. In the present study, we elucidated the local and systemic effects of plasmid construct рBud-coVEGF165-coFGF2 injected into the epineurium of intact rat sciatic nerve. Results of histological examination of sciatic nerve and multiplex immunoassays of serum showed the absence of immunogenicity and biosafety of plasmid рBud-coVEGF165-coFGF2. Moreover, local administration of plasmid DNA construct resulted in significantly decreased levels of pro-inflammatory cytokines in the peripheral blood, including tumor necrosis factor α(TNFα) and interleukin-12, and significantly increased levels of cytokines and chemokines including Regulated upon Activation, Normal T Cell Expressed and Presumably Secrete(RANTES), epidermal growth factor, interleukin-2, and monocyte chemoattractant protein 1. These changes in the peripheral blood on day 7 after injection of plasmid construct рBud-coVEGF165-coFGF2 show that the plasmid construct has systemic effects and may modulate immune response. At the same time, reverse transcriptionpolymerase chain reaction revealed transient expression of coFGF2, coVEGF165, ratFGF2 and ratVEGFA with direct transport of transcripts from distal part to proximal part of the sciatic nerve. Immunohistochemical staining revealed prolonged presence of VEGFA in sciatic nerve till 14 days post-injection. These findings suggest that local administration of plasmid construct рBud-coVEGF165-coFGF2 at a concentration of 30 ng/μL results in the formation of pro-angiogenic stimuli and, and the plasmid construct, used as a drug for gene therapy, might potentially facilitate regeneration of the sciatic nerve. The study was approved by the Animal Ethics Committee of Kazan Federal University, procedures were approved by the Local Ethics Committee(approval No. 5) on May 27, 2014. 展开更多
关键词 CHEMOKINES CYTOKINES fibroblast growth factor gene therapy growth factors peripheral nerve system sciatic nerve regeneration vascular endothelial growth factor
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Dual growth factor-immobilized microspheres for tissue reinnervation
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作者 Tae Ho Kim Se Heang Oh +1 位作者 Dan Bi An Jin Ho Lee 《Asian Journal of Pharmaceutical Sciences》 SCIE CAS 2016年第1期154-155,共2页
It has been reported that various progenitor cells or stem cells and continuously released bioactive molecules can enhance the regeneration of muscles and thus help to treat chronic degenerative diseases,such as urina... It has been reported that various progenitor cells or stem cells and continuously released bioactive molecules can enhance the regeneration of muscles and thus help to treat chronic degenerative diseases,such as urinary/fecal incontinence and erectile dysfunction.However,the regeneration ofmuscles alone cannot be a fundamental cure of chronic degenerative diseases,because regenerated muscles with insufficient nerve connections subsequently lead tomuscle atrophy[1]. 展开更多
关键词 Microsphere Basic fibroblast growth factor(BFGF) nerve growth factor(ngf) NEUROGENIC differentiation nerve regeneration
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CLONING AND SEQUENCING OF MATURED FRAGMENT OF HUMAN NEVER GROWTH FACTOR GENE
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作者 马巍 吴玲 +4 位作者 王德利 刘淼 任惠民 杨广笑 王全颖 《Journal of Pharmaceutical Analysis》 SCIE CAS 2003年第1期62-65,共4页
Objective Molecular cloning and sequencing of the human matured fragment of human nerve growth factor(NGF) gene. Methods Extracting the human genomic DNA from the white blood cells as templates, the gene of NGF was ... Objective Molecular cloning and sequencing of the human matured fragment of human nerve growth factor(NGF) gene. Methods Extracting the human genomic DNA from the white blood cells as templates, the gene of NGF was cloned by using PCR and T vector cloning method. Screening the positive clones and identified by the restriction enzymes, and then the cloned amplified fragment was sequenced and analyzed. Results DNA sequence comparison the cloned gene of NGF with the GenBank (V01511) sequence demonstrated that both of sequences were identical, 354bp length. Conclusion Cloning the NGF gene from the human genomic DNA has paved the way for further study on gene therapy of nerve system injury. 展开更多
关键词 polymerase chain reaction (PCR) T vector nerve growth factor (ngf)
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GENE CLONING OF HUMAN NERVE GROWTH FACTOR (hNGF) 被引量:1
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作者 华仲慰 刘宏迪 +3 位作者 郭建荣 余云开 吴晓军 李玉书 《Chinese Science Bulletin》 SCIE EI CAS 1992年第13期1130-1133,共4页
NGF is one of the few endogenous neurotrophic factors which have been clarified in structure and gene sequence. The β subunit of NGF (β-NGF) has been proved to be effective in promoting normal development and differ... NGF is one of the few endogenous neurotrophic factors which have been clarified in structure and gene sequence. The β subunit of NGF (β-NGF) has been proved to be effective in promoting normal development and differentiation of certain neurons in both central and peripheral nervous systemst. It has also shown to play 展开更多
关键词 nerve growth factor POLYMERASE CHAIN reaction gene CLONING
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双叶清肺止咳糖浆止咳药效学及对大鼠感染后支气管模型BALF中P物质、CGRP、NGF的影响 被引量:1
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作者 程慧 黄德红 +3 位作者 李林 张荔 宋侨 吴勇 《亚太传统医药》 2023年第1期34-37,共4页
目的:研究双叶清肺止咳糖浆的祛痰、抗炎作用及其作用机制。方法:通过大鼠玻璃毛细管排痰实验和小鼠气管酚红排泌实验,观察双叶清肺止咳糖浆的祛痰作用;通过小鼠耳肿胀实验观察双叶清肺止咳糖浆的抗炎作用,通过小剂量脂多糖(LPS)诱导革... 目的:研究双叶清肺止咳糖浆的祛痰、抗炎作用及其作用机制。方法:通过大鼠玻璃毛细管排痰实验和小鼠气管酚红排泌实验,观察双叶清肺止咳糖浆的祛痰作用;通过小鼠耳肿胀实验观察双叶清肺止咳糖浆的抗炎作用,通过小剂量脂多糖(LPS)诱导革兰阴性菌感染,建立大鼠感染后支气管模型,用ELISA法检测空白组、双叶清肺止咳糖浆高、中、低剂量组、阳性对照组左肺BALF中P物质(SP)、降钙素基因相关肽(CGRP)、鼠神经生长因子(NGF)的含量。结果:(1)大鼠排痰实验中,双叶清肺止咳糖浆高、中剂量组、氯化铵组大鼠排痰量较空白组增加,差异显著(P<0.01);(2)小鼠气管酚红排泌实验中,双叶清肺止咳糖浆高剂量组、氯化铵组、急支糖浆组能升高排泌酚红浓度,与空白组比较,差异显著(P<0.05,P<0.01);(3)小鼠耳肿胀实验中,双叶清肺止咳糖浆高剂量组、醋酸泼尼松组、急支糖浆组耳肿胀度较空白组降低,差异显著(P<0.05,P<0.01);(4)模型实验中,与正常组比较,模型组SP、CGRP、NGF的含量明显升高,双叶清肺止咳糖浆高、中剂量组、美敏伪麻溶液组SP、CGRP、NGF的含量与模型组比较显著降低,差异具有统计学意义(P<0.05,P<0.01)。结论:双叶清肺止咳糖浆能促进排痰,减轻炎症反应,减少大鼠咳嗽次数,保护受损炎症组织,其机制可能与改善大鼠SP和CGRP、NCF表达有关。 展开更多
关键词 双叶清肺止咳糖浆 感染后支气管炎模型 P物质 降钙素基因相关肽 鼠神经生长因子
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Effect of Murine Nerve Growth Factor and Sodium Ganglioside on the Levels of NF-kB p56,TLR-4 and MyD88 in Hippocampus of Epileptic Rats
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作者 RAO Zhi-hui LIANG Hai-ying XIANG Yan-chun 《Chinese Journal of Biomedical Engineering(English Edition)》 CAS 2023年第3期124-130,共7页
Objective:Epilepsy is a prevalent neurological condition,and NF-kB,TLR-4,and MyD88 are significant contributors to its development.Murine nerve growth factor(NGF)and monosialotetrahexosylganlioside sodium for injectio... Objective:Epilepsy is a prevalent neurological condition,and NF-kB,TLR-4,and MyD88 are significant contributors to its development.Murine nerve growth factor(NGF)and monosialotetrahexosylganlioside sodium for injection(MSI)are essential neurotrophic medications,yet their regulatory mechanism in the pathogenesis of epilepsy remains uncertain.The aim of this research was to examine the impacts of NGF and MSI on nuclear factor-kB(NF-kB)p65,toll-like receptor 4(TLR-4),and myeloid differentiation primary response gene 88(MyD88)in order to clarify their mechanisms of action in the management of epilepsy.Methods:A total of 40 SD rats were randomly assigned to one of five groups:blank,model,NGF model,MSI model,and NGF+MSI model.Epileptic rat models were induced through intraperitoneal injection of lithium chloride and pilocarpine solution.The rats'body mass and behavioral traits were subsequently observed.The Western blotting technique was utilized to detect the levels of NF-kB p65,TLR-4,and MyD88.Results:The findings indicated a more pronounced increase in body mass among the four groups prior to sacrifice,as compared to the model group.Notably,the NGF+MSI model group exhibited significant enhancements in food intake,activity,and body weight.The frequency of seizures in NGF group,MSI group,and NGF+MSI group were(5.33±1.15),(4.33±1.03),and(2.66±1.33)times/7 d,respectively,with neuronal apoptosis rates being(23.17±2.91),(21.38±3.07),(18.19±2.14)%times/7 d,respectively,which were lower than those in the model group.The levels of NF-kB p56,TLR-4,and MyD88 in the hippocampus were reduced in the model group compared to the three treatment groups.Furthermore,the expression levels in the NGF+MSI model group closely resembled those in the control group(P>0.05).Conclusion:Thorough examination revealed that NGF and MSI,either individually or in conjunction,were capable of suppressing the activation of the NF-kB pathway and enhancing the TLR-4/MyD88 signaling pathway to exert an antiepileptic influence.Furthermore,the combined administration of NGF and MSI demonstrated greater efficacy in safeguarding hippocampal neurons in epileptic rats. 展开更多
关键词 murine nerve growth factor(ngf) ganglioside sodium epilepsy hippocampal tissue neurons
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Expression of human nerve growth factor βgene in central nervous system mediated by recombinant adeno-associated viruses type-2 vector 被引量:1
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作者 高凯 吴勇杰 +2 位作者 吴小兵 饶春明 王军志 《Chinese Medical Journal》 SCIE CAS CSCD 2004年第9期1370-1376,共7页
Background Neurone atrophy and loss are major causes of chronic neurodegenerative disorders such as Alzheimer’s disease. Despite many pharmacotherapies for neurodegeneration, there are no accepted treatments. We in... Background Neurone atrophy and loss are major causes of chronic neurodegenerative disorders such as Alzheimer’s disease. Despite many pharmacotherapies for neurodegeneration, there are no accepted treatments. We investigated the feasibility of human nerve growth factor β (hNGFβ) gene expression mediated by recombinant adeno-associated viruses type-2 (rAAV-2) vector in the central nervous system (CNS) after blood brain barrier (BBB) disruption.Methods rAAV-2 containing hNGFβ gene was constructed. The ability of hNGFβ gene mediated by rAAV-2 vector (rAAV-2/hNGFβ) to transfect cells in vitro was confirmed by both ELISA and bioassay of hNGFβ in the culture supernatant of BHK-21 cells infected by rAAV-2/hNGFβ. rAAV-2/hNGFβ and rAAV-2/green fluorescence protein (GFP) were administrated separately to rat brains through internal carotid intubation after BBB disruption with hypertonic mannitol. Brain hNGFβ concentration was measured by ELISA and GFP in brain sections was examined by laser scan confocal microscope.Results After 48 hours, hNGFβ content in supernatant was up to (188.0±28.6) pg/ml when BHK-21 cells were infected by rAAV-2/hNGFβ at multiplicity of infection (MOI)1.0×106 vector genome. Neurone fibre outgrowths were obvious in dorsal root ganglion neurone assays by adding serum free culture medium harvested from BHK-21 cells exposed to rAAV-2/hNGFβ. Whole brain hNGFβ content in rAAV-2/hNGFβ transferred group was up to (636.2±140.6) pg/ml. hNGFβ content of BBB disruption in rAAV-2/hNGFβ infused group increased significantly compared to the control group (P<0.05). GFP expression was clearly observed in brain sections of rAAV-2/GFP transferred group.Conclusion rAAV-2/hNGFβ successfully expresses in the CNS after BBB disruption induced by hypertonic mannitol. 展开更多
关键词 human nerve growth factor β adeno-associated virus gene therapy blood brain barrier
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NGF对坐骨神经损伤后腰髓与损伤神经MBP含量变化的影响 被引量:13
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作者 曾琳 杨恒文 +1 位作者 邵阳 伍亚民 《第三军医大学学报》 CAS CSCD 北大核心 2002年第3期326-327,共2页
目的 探讨大鼠周围神经损伤后相应神经与脊髓组织髓鞘碱性蛋白 (Myelinbasicprotein ,MBP)含量变化及神经生长因子 (NGF)的影响。方法 Wistar大鼠行单侧坐骨神经切断 ,断端采用硅胶管桥接 ,管内注入NGF ,应用酶联免疫吸附法测定腰段... 目的 探讨大鼠周围神经损伤后相应神经与脊髓组织髓鞘碱性蛋白 (Myelinbasicprotein ,MBP)含量变化及神经生长因子 (NGF)的影响。方法 Wistar大鼠行单侧坐骨神经切断 ,断端采用硅胶管桥接 ,管内注入NGF ,应用酶联免疫吸附法测定腰段脊髓和损伤坐骨神经组织MBP含量的变化 ,实验分为Ⅰ组 :生理盐水对照 ;Ⅱ组 :硅胶管内给NGF ;Ⅲ组 :硅胶管内给NGF +每日肌肉注射NGF(5 0 0ng/kg连续 2周 )。结果 治疗组之间比较无统计学意义 ;治疗组与对照组相比较有非常显著性差异 (P <0 0 1) ;治疗组2 4h、2周时MBP含量较伤前显著升高 (P <0 0 1) ,4周恢复到伤前水平。结论 NGF治疗能减少MBP含量 。 展开更多
关键词 坐骨神经损伤 神经生长因子 ngf 髓鞘碱性蛋白 MBP 含量 影响 腰髓 损伤神经
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丁基苯酞对大鼠缺血脑组织NGF及BDNF表达的影响 被引量:11
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作者 孔双艳 李其富 +1 位作者 羊洁 何俐 《四川大学学报(医学版)》 CAS CSCD 北大核心 2007年第3期400-403,407,共5页
目的研究丁基苯酞对大鼠缺血脑组织中脑源性神经生长因子(BDNF)和神经生长因子(NGF)表达的影响。方法健康雄性SD大鼠,用大鼠大脑中动脉线栓法(MCAO)建立永久性缺血模型,按照Zea-Longa的方法对动物的神经功能进行评分,选取1~3分的大鼠... 目的研究丁基苯酞对大鼠缺血脑组织中脑源性神经生长因子(BDNF)和神经生长因子(NGF)表达的影响。方法健康雄性SD大鼠,用大鼠大脑中动脉线栓法(MCAO)建立永久性缺血模型,按照Zea-Longa的方法对动物的神经功能进行评分,选取1~3分的大鼠按随机数字表随机分成2组:丁基苯酞治疗组(A组),大脑中动脉永久缺血对照组(B组),每组各20只。A组于术后予以丁基苯酞,每天2次,每次25mg/kg,B组给予相应剂量食用油灌胃给药,72h后行神经功能评分,然后处死,分别取脑梗死周围、海马区和梗死区脑组织作免疫组化染色检测BDNF、NGF蛋白表达变化,原位杂交检测BDNF mRNA、NGF mRNA的表达。结果丁基苯酞治疗组神经功能评分(1.35±0.81)低于对照组(1.75±0.55),差异有统计学意义(P=0.04)。丁基苯酞治疗组BDNF和NGF蛋白BDNF mRNA和NGF mRNA在梗死区周围和海马区表达均高于对照组,差异有统计学意义(P<0.05),在梗死区差异均无统计学意义(P>0.05)。结论丁基苯酞可上调大鼠梗死区周围和海马区缺血脑组织中BDNF和NGF的表达,并可能通过此机制起到保护作用。 展开更多
关键词 缺血性脑血管病 线栓法大脑中动脉栓塞模型 丁基苯酞 神经生长因子(ngf) 脑源性神经 生长因子(BDNF)
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