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| 1 | Constraint-induced movement therapy enhances angiogenesis and neurogenesis after cerebral ischemia/reperfusion显示文摘Constraint-induced movement therapy after cerebral ischemia stimulates axonal growth by decreasing expression levels of Nogo-A,RhoA,and Rho-associated kinase(ROCK)in the ischemic boundary zone.However,it remains unclear if there are any associations between the Nogo-A/RhoA/ROCK pathway and angiogenesis in adult rat brains in pathological processes such as ischemic stroke.In addition,it has not yet been reported whether constraint-induced movement therapy can promote angiogenesis in stroke in adult rats by overcoming Nogo-A/RhoA/ROCK signaling.Here,a stroke model was established by middle cerebral artery occlusion and reperfusion.Seven days after stroke,the following treatments were initiated and continued for 3 weeks:forced limb use in constraint-induced movement therapy rats(constraint-induced movement therapy group),intraperitoneal infusion of fasudil(a ROCK inhibitor)in fasudil rats(fasudil group),or lateral ventricular injection of NEP1-40(a specific antagonist of the Nogo-66 receptor)in NEP1-40 rats(NEP1-40 group).Immunohistochemistry and western blot assay results showed that,at 2 weeks after middle cerebral artery occlusion,expression levels of RhoA and ROCK were lower in the ischemic boundary zone in rats treated with NEP1-40 compared with rats treated with ischemia/reperfusion or constraint-induced movement therapy alone.However,at 4 weeks after middle cerebral artery occlusion,expression levels of RhoA and ROCK in the ischemic boundary zone were markedly decreased in the NEP1-40 and constraint-induced movement therapy groups,but there was no difference between these two groups.Compared with the ischemia/reperfusion group,modified neurological severity scores and foot fault scores were lower and time taken to locate the platform was shorter in the constraint-induced movement therapy and fasudil groups at 4 weeks after middle cerebral artery occlusion,especially in the constraint-induced movement therapy group.Immunofluorescent staining demonstrated that fasudil promoted an immune response of nerve-regeneration-related markers(BrdU in combination with CD31(platelet endothelial cell adhesion molecule),Nestin,doublecortin,NeuN,and glial fibrillary acidic protein)in the subventricular zone and ischemic boundary zone ipsilateral to the infarct.After 3 weeks of constraint-induced movement therapy,the number of regenerated nerve cells was noticeably increased,and was accompanied by an increased immune response of tight junctions(claudin-5),a pericyte marker(a-smooth muscle actin),and vascular endothelial growth factor receptor 2.Taken together,the results demonstrate that,compared with fasudil,constraint-induced movement therapy led to stronger angiogenesis and nerve regeneration ability and better nerve functional recovery at 4 weeks after cerebral ischemia/reperfusion.In addition,constraint-induced movement therapy has the same degree of inhibition of RhoA and ROCK as NEP1-40.Therefore,constraint-induced movement therapy promotes angiogenesis and neurogenesis after cerebral ischemia/reperfusion injury,at least in part by overcoming the Nogo-A/RhoA/ROCK signaling pathway.All protocols were approved by the Institutional Animal Care and Use Committee of China Medical University,China on December 9,2015(approval No.2015 PS326 K). | Zhi-Yong Zhai Juan Feng | 2019 | Neural Regeneration Research2019，14，10： | 22 |
| 2 | Prevention of bone loss by injection of insulin-like growth factor-1 after sciatic neurectomy in rats显示文摘 | SUN Hai-biao CHEN Jun-chang | 2013 | Chinese Journal of Traumatology2013，16，3： | 19 |
| 3 | Increased expression of brain-derived neurotrophic factor is correlated with visceral hypersensitivity in patients with diarrheapredominant irritable bowel syndrome显示文摘BACKGROUND Visceral hypersensitivity is considered to play a vital role in the pathogenesis of irritable bowel syndrome(IBS). Neurotrophins have drawn much attention in IBS recently. Brain-derived neurotrophic factor(BDNF) was found to mediate visceral hypersensitivity via facilitating sensory nerve growth in pre-clinical studies. We hypothesized that BDNF might play a role in the pathogenesis of diarrhea-predominant IBS(IBS-D).AIM To investigate BDNF levels in IBS-D patients and its role in IBS-D pathophysiology.METHODS Thirty-one IBS-D patients meeting the Rome IV diagnostic criteria and 20 ageand sex-matched healthy controls were recruited. Clinical and psychological assessments were first conducted using standardized questionnaires. Visceral sensitivity to rectal distension was tested using a high-resolution manometry system. Colonoscopic examination was performed and four mucosal pinch biopsies were taken from the rectosigmoid junction. Mucosal BDNF expression and nerve fiber density were analyzed using immunohistochemistry. Mucosal BDNF mRNA levels were quantified by quantitative real-time polymerase chain reaction. Correlations between these parameters were examined.RESULTS The patients had a higher anxiety score [median(interquartile range), 6.0(2.0-10.0) vs 3.0(1.0-4.0), P = 0.003] and visceral sensitivity index score [54.0(44.0-61.0)vs 21.0(17.3-30.0), P < 0.001] than controls. The defecating sensation threshold[60.0(44.0-80.0) vs 80.0(61.0-100.0), P = 0.009], maximum tolerable threshold[103.0(90.0-128.0) vs 182.0(142.5-209.3), P < 0.001] and rectoanal inhibitory reflex threshold [30.0(20.0-30.0) vs 30.0(30.0-47.5), P = 0.032] were significantly lower in IBS-D patients. Intestinal mucosal BDNF protein [3.46 E-2(3.06 E-2-4.44 E-2) vs3.07 E-2(2.91 E-2-3.48 E-2), P = 0.031] and mRNA [1.57(1.31-2.61) vs 1.09(0.74-1.42), P = 0.001] expression and nerve fiber density [4.12 E-2(3.07 E-2-7.46 E-2) vs1.98 E-2(1.21 E-2-4.25 E-2), P = 0.002] were significantly elevated in the patients.Increased BDNF expression was positively correlated with abdominal pain and disease severity and negatively correlated with visceral sensitivity parameters.CONCLUSION Elevated mucosal BDNF may participate in the pathogenesis of IBS-D via facilitating mucosal nerve growth and increasing visceral sensitivity. | Yu Zhang Geng Qin De-Rong Liu Yan Wang Shu-Kun Yao | 2019 | World Journal of Gastroenterology2019，25，2： | 14 |
| 4 | A comparative study on the transplantation of different concentrations of human umbilical mesenchymal cells into diabetic rats显示文摘AIM: To observe the effects of intravitreal injections of different concentrations of human umbilical mesenchymal stem cells on retinopathy in rats with diabetes mellitus.METHODS: Healthy and adult male Sprague-Dawley(SD) rats were randomly assigned to a normal control group(group A), a diabetic retinopathy(DR) blank control group(group B), a high-concentration transplantation group(group C), a low-concentration transplantation group(group D) and a placebo transplantation group(group E). The expression of nerve growth factor(NGF)protein in the retinal layers was detected by immunohistochemical staining at 2, 4, 6 and 8wk.RESULTS: The expression of NGF was positive in group A and most positive in the retinal ganglion cell layer. In groups B and E, the expression of NGF was positive 2wk after transplantation and showed an increase in all layers. However, the level of expression had decreased in all layers at 4wk and was significantly reduced at 8wk. In groups C and D, the expression of NGF had increased at 2wk and continued to increase up to 8wk. The level of expression in group C was much higher than that in group D.CONCLUSION: DR can be improved by intravitreal injection of human umbilical mesenchymal stem cells.High concentrations of human umbilical mesenchymal stem cells confer a better protective effect on DR than low concentrations. | Jia-Hui Kong Dan Zheng Song Chen Hong-Tao Duan Yue-Xin Wang Meng Dong Jian Song | 2015 | International Journal of Ophthalmology(English edition)2015，8，2： | 9 |
| 5 | Novel miRNA, miR-sc14, promotes Schwann cell proliferation and migration显示文摘MicroRNAs refer to a class of endogenous,short non-coding RNAs that mediate numerous biological functions.MicroRNAs regulate various physiological and pathological activities of peripheral nerves,including peripheral nerve repair and regeneration.Previously,using a rat sciatic nerve injury model,we identified many functionally annotated novel microRNAs,including miR-sc14.Here,we used real-time reverse transcription-polymerase chain reaction to examine miR-sc14 expression in rat sciatic nerve stumps.Our results show that miRsc14 is noticeably altered following sciatic nerve injury,being up-regulated at 1 day and diminished at 7 days.EdU and transwell chamber assay results showed that miR-sc14 mimic promoted proliferation and migration of Schwann cells,while miR-sc14 inhiThe study was approved by the Jiangsu Provincial Laboratory Animal Management Committee,China on March 4,2015(approval No.20150304-004).bitor suppressed their proliferation and migration.Additionally,bioinformatic analysis examined potential target genes of miR-sc14,and found that fibroblast growth factor receptor 2 might be a potential target gene.Specifically,our results show changes of miR-sc14 expression in the sciatic nerve of rats at different time points after nerve injury.Appropriately,up-regulation of miR-sc14 promoted proliferation and migration of Schwann cells.Consequently,miR-sc14 may be an intervention target to promote repair of peripheral nerve injury.The study was approved by the Jiangsu Provincial Laboratory Animal Management Committee,China on March 4,2015(approval No.20150304-004). | Xi-Meng Ji Shan-Shan Wang Xiao-Dong Cai Xing-Hui Wang Qian-Yan Liu Pan Wang Zhang-Chun Cheng Tian-Mei Qian | 2019 | Neural Regeneration Research2019，14，9： | 6 |
| 6 | Uncoupling neurotrophic function from nociception of nerve growth factor: what can be learned from a rare human disease?显示文摘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. | Kijung Sung Wanlin Yang Chengbiao Wu | 2019 | Neural Regeneration Research2019，14，4： | 5 |
| 7 | Fresh human amniotic membrane effectively promotes the repair of injured common peroneal nerve显示文摘Suture and autologous nerve transplantation are the primary therapeutic measures for completely severed nerves. However, imbalances in the microenvironment and adhesion of surrounding tissues can affect the quality of nerve regeneration and repair. Previous studies have shown that human amniotic membrane can promote the healing of a variety of tissues. In this study, the right common peroneal nerve underwent a 5-mm transection in rats. Epineural nerve repair was performed using 10/0 non-absorbable surgical suture. The repair site was wrapped with a two-layer amniotic membrane with α-cyanoacrylate rapid medical adhesive after suture. Hindlimb motor function was assessed using footprint analysis. Conduction velocity of the common peroneal nerve was calculated by neural electrical stimulation. The retrograde axoplasmic transport of the common peroneal nerve was observed using fast blue BB salt retrograde fluorescent staining. Hematoxylin- eosin staining was used to detect the pathological changes of the common peroneal nerve sputum. The mRNA expression of axon regeneration-related neurotrophic factors and inhibitors was measured using real-time polymerase chain reaction. The results showed that the amniotic membrane significantly improved the function of the injured nerve;the toe spread function rapidly recovered, the nerve conduction velocity was restored, and the number of fast blue BB salt particles were increased in the spinal cord. The amniotic membrane also increased the recovery rate of the tibialis anterior muscle and improved the tissue structure of the muscle. Meanwhile, mRNA expression of nerve growth factor, growth associated protein-43, collapsin response mediator protein-2, and brain-derived neurotrophic factor recovered to near-normal levels, while Lingo-1 mRNA expression decreased significantly in spinal cord tissues. mRNA expression of glial-derived neurotrophic factor did not change significantly. Changes in mRNA levels were more significant in amniotic-membrane-wrapping-treated rats compared with model and nerve sutured rats. These results demonstrate that fresh amniotic membrane wrapping can promote the functional recovery of sutured common peroneal nerve via regulation of expression levels of neurotrophic factors and inhibitors associated with axonal regeneration. The study was approved by the Committee on Animal Research and Ethics at the Affiliate Hospital of Zunyi Medical University, China (approval No. 112) on December 1, 2017. | Zhong-Yuan Zhang Jin Yang Zhen-Hai Fan Da-Li Wang Yu-Ying Wang Tao Zhang Li-Mei Yu Chang-Yin Yu | 2019 | Neural Regeneration Research2019，14，12： | 5 |
| 8 | Clinical significance of nerve growth factor and tropomyosin-receptor-kinase signaling pathway in intrahepatic cholangiocarcinoma显示文摘AIM:To investigate the correlation between nerve growth factor-tropomyosin-receptor-kinase(NGF-TrkA)signaling pathway and prognosis in intrahepatic cholangiocarcinoma(IHCC).METHODS:NGF and TrkA expression in 83 samples of IHCC was assessed by immunohistochemistry.Correlations between NGF-TrkA expression and clinicopathological features were analyzed byχ2 test.Moreover,we evaluated the association between NGF-TrkA and overall survival by univariate and multivariate analysis.With experiments in vitro,we investigated the crucial role of NGF-TrkA on proliferation and invasion of IHCC cells with recombinant NGF-βstimulation.RESULTS:We found that NGF and TrkA expression was significantly related with differentiation(P=0.024)and intraneural invasion(P=0.003),respectively.Additionally,double higher expression of NGF and TrkA was identified as an independent prognostic factor in IHCC(P=0.003).Moreover,we demonstrated that NGF-TrkA signaling pathway can promote IHCC proliferation and invasion.CONCLUSION:NGF-TrkA double higher expression is an independent prognostic factor in IHCC.NGF-TrkA pathway can promote IHCC progression,indicating that NGF-TrkA may become a potential drug target. | Xiao-Qing Yang Yun-Fei Xu Sen Guo Yi Liu Shang-Lei Ning Xiao-Fei Lu Hui Yang Yu-Xin Chen | 2014 | World Journal of Gastroenterology2014，20，14： | 4 |
| 9 | Vascular endothelial growth factor A promotes platelet adhesion to collagen Ⅳ and causes early brain injury after subarachnoid hemorrhage显示文摘The role of vascular endothelial growth factor A in platelet adhesion in cerebral microvessels in the early stage of subarachnoid hemorrhage remains unclear.In this study,the endovascular puncture method was used to produce a rat model of subarachnoid hemorrhage.Then,30 minutes later,vascular endothelial growth factor A antagonist anti-vascular endothelial growth factor receptor 2 antibody,10μg,was injected into the right ventricle.Immunohistochemistry and western blot assay were used to assess expression of vascular endothelial growth factor A,occludin and claudin-5.Immunohistochemical double labeling was conducted to examine co-expression of GP Ⅰa-Ⅱ integrin and type Ⅳ collagen.TUNEL was used to detect apoptosis in the hippocampus.Neurological score was used to assess behavioral performance.After subarachnoid hemorrhage,the expression of vascular endothelial growth factor A increased in the hippocampus,while occludin and claudin-5 expression levels decreased.Co-expression of GP Ⅰa-Ⅱ integrin and type Ⅳ collagen and the number of apoptotic cells increased,whereas behavioral performance was markedly impaired.After treatment with anti-vascular endothelial growth factor receptor 2 antibody,occludin and claudin-5 expression recovered,while co-expression of GP Ⅰa-Ⅱ integrin and type Ⅳ collagen and the number of apoptotic cells decreased.Furthermore,behavioral performance improved notably.Our findings suggest that increased vascular endothelial growth factor A levels promote platelet adhesion and contribute to early brain injury after subarachnoid hemorrhage.This study was approved by the Biomedical Ethics Committee,Medical College of Xi’an Jiaotong University,China in December 2015. | Zun-Wei Liu Jun-Jie Zhao Hong-Gang Pang Jin-Ning Song | 2019 | Neural Regeneration Research2019，14，10： | 4 |
| 10 | Effects of nerve growth factor on nitric oxide-mediated neurotoxicity in primary cortical cultures显示文摘ObjectiveToobservetheefectsofnervegrowthfactor(NGF)onnitricoxide(NO)releaseandconstitutivenitricoxidesynthase(cNOS)geneexpres... | 吴俊芳 张均田 | 1999 | Chinese Medical Journal1999，，5： | 3 |
| 11 | Mechanisms by which fibroblast growth factor 20 improves motor performance in a mouse model of Parkinson’s disease显示文摘Genome-wide studies have reported that Parkinson's disease is associated with abnormal expression of various growth factors. In this study, male C57BL/6 mice aged 10 weeks were used to establish Parkinson's disease models using an intraperitoneal injection of 60 mg/kg 1-methyl- 4-phenyl-1,2,3,6-tetrahydropyridine. 28 days later, 10 or 100 ng fibroblast growth factor 20 was injected intracerebroventricularly. The electrophysiological changes in the mouse hippocampus were recorded using a full-cell patch clamp. Expression of Kv4.2 in the substantia nigra was analyzed using a western blot assay. Serum malondialdehyde levels were analyzed by enzyme-linked immunosorbent assay. The motor coordination of mice was evaluated using the rotarod test. The results showed that fibroblast growth factor 20 decreased A-type potassium current in neurons of the substantia nigra, increased long-term potentiation amplitude in the hippocampus, and downregulated Kv4.2 expression. A high dose of fibroblast growth factor 20 reduced serum malondialdehyde levels and enhanced the motor coordination of mice. These findings confirm that fibroblast growth factor 20 has a therapeutic effect on the toxicity induced by l-methyl-4-phenyl-l,2,3s6-tetrahydropyridine, and its mechanism of action is associated with the inhibition of A-type K^+ currents and Kv4.2 expression. All animal procedures were approved by the Animal Care and Use Committee of Qilu Hospital of Shandong University, China in 2017 (approval No. KYLL-2017-0012). | Ai-Qin Wang Li-Na Kong Ming-Zhu Meng Xiu-He Zhao Si Chen Xiao-Tang Wang | 2019 | Neural Regeneration Research2019，14，8： | 1 |
| 12 | GENE CLONING OF HUMAN NERVE GROWTH FACTOR (hNGF)显示文摘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 | 华仲慰 刘宏迪 郭建荣 余云开 吴晓军 李玉书 | 1992 | Chinese Science Bulletin1992，37，13： | 1 |
| 13 | Diabetic neuropathy research: from mouse models to targets for treatment显示文摘Diabetic neuropathy is one of the most serious complications of diabetes, and its increase shows no sign of stopping. Furthermore, current clinical treatments do not yet approach the best effectiveness. Thus, the development of better strategies for treating diabetic neuropathy is an urgent matter. In this review, we first discuss the advantages and disadvantages of some major mouse models of diabetic neuropathy and then address the targets for mechanism-based treatment that have been studied. We also introduce our studies on each part. Using stem cells as a source of neurotrophic factors to target extrinsic factors of diabetic neuropathy, we found that they present a promising treatment. | Vuong M. Pham Shinji Matsumura Tayo Katano Nobuo Funatsu Seiji Ito | 2019 | Neural Regeneration Research2019，14，11： | 1 |
| 14 | Improving the protective effects of a FGF for peripheral nerve injury repair using sulfated chitooligosaccharides显示文摘Injury to the peripheral nerves can result in temporary or life-long neuronal dysfunction and subsequent economic or social disability. Acidic fibroblast growth factor(a FGF) promotes the growth and survival of neurons and is a possible treatment for peripheral nerve injury. Yet,the actual therapeutic utility of a FGF is limited by its short half-life and instability in vivo. In the present study,we prepared sulfated chitooligosaccharides(SCOS),which have heparinlike properties,to improve the bioactivity of a FGF. We investigated the protective effects of SCOS with or without a FGF on RSC96 cells exposed to Na2 S2 O4 hypoxia/reoxygenation injury. Cell viability was measured by MTT assay and cytotoxicity induced by Na2 S2 O4 was assessed by lactate dehydrogenase(LDH) release into the culture medium. Pretreatment with a FGF and SCOS dramatically decreased LDH release after injury compared to pretreatment with a FGF or SCOS alone. We subsequently prepared an a FGF/SCOS thermo-sensitive hydrogel with poloxamer and examined its effects in vivo. Paw withdrawal thresholds and thermal withdrawal latencies were measured in rats with sciatic nerve injury. Local injection of the a FGF/SCOS hydrogels(a FGF: 40,80 μg/kg) increased the efficiency of sciatic nerve repair compared to a FGF(80 μg/kg) hydrogel alone. Especially a FGF/SCOS thermo-sensitive hydrogel decreased paw withdrawal thresholds from 117.75 ± 8.38(g,4 d) to 65.74 ± 3.39(g,10 d),but a FGF alone group were 140.58 ± 27.54(g,4 d) to 89.12 ± 5.60(g,10 d)(a FGF dose was 80 μg/kg,P < 0.05,n = 8). The thermal withdrawal latencies decreased from 11.61 ± 2.26(s,4 d) to 2.37 ±0.67(s,10 d). However,a FGF alone group were from 17.69 ± 1.47(s,4 d) to4.65 ± 1.73(s,10 d)(P < 0.05,n = 8). Furthermore,the a FGF/SCOS hydrogels also exhibited good biocompatibility in mice. In summary,SCOS improved the protective effects of a FGF in RSC96 cells injured with Na2S2O4 and increased the efficiency of nerve repair and recovery of function in rats with sciatic nerve injury. These findings pave an avenue for the development of novel prophylactic and therapeutic strategies for peripheral nerve injury. | Yanmei Liu Fenglin Yu Beibei Zhang Meng Zhou Yu Bei Yifan Zhang Jianzhong Tang Yan Yang Yadong Huang Qi Xiang Yueping Zhao Qian Liang Yang Liu | 2019 | Asian Journal of Pharmaceutical Sciences2019，14，5： | 0 |
| 15 | Effect of siRNA interference on nerve growth factor in intervertebral disc inflammation rats显示文摘Objective:To investigate the inhibition effect of siRNA interference on NGF induced by inflammatory factor IL-6,and JUL—1 so as to provide novel targets for clinical treatment of discogenic low back pain.Methods:The intervertebral disc nucleus and annulus fibrosus cells of rats were separated-The cells were co-cultured with different concentrations(10 nmol/L,20nmol/L,50 nmol/L,100 nmol/L)of IL-6 and IL-1β.The NGF-siRNA was leaded into the cocultured cells with its import ability assessed by flow cytometry instrument tests,hefore and after which the NCF mRNA expression was detected by real-time Q-PCR and the NGF content was detected by ELISA.Results:Flow cytometry instrument test results showed that the NGFsiRNA cell conversion rate was 99.8%.Real-time Q-PCR detection results showed that compared with negative control group,the NGF mRNA expression of co-cultured cells treated by 10 nmol/L,20 nmol/L,50 nmol/L,100 nmol/L IL-6 and IL-1βwere respectively raised 3.4,3.7,4.7,3.7 times which were all significantly down-regulated after the import of NGF-siRNA.EILSA detection results showed that compared with negative control group,the NGF content of cocultured medium treated by 10 nmol/L,20 nmol/L,50 nmol/L,100 nmol/L I-L6 and IL-1βwere respectively raised 2.9,3.3,4.5,7.4 times which were all significantly decreased after the import of NGF-siRNA.Conclusions:These molecular biological results suggest that inflammatory factor IL-6 and IL-1βcould stimulate NCF on intervertebral disc cells in vitro culture model and its efficiency is concentration dependent,while siRNA interference can inhibit the stimulation effect of IL-6 and IL-1βon intervertebral disc cell,which provides a new targets for the clinical treatment of discogenic low back pain. | Ming-Lei Lang Ai-Lin Qin Jian-Min Li Peng Fu | 2014 | Asian Pacific Journal of Tropical Medicine2014，7，9： | 0 |
| 16 | Immunohistochemical study of P^(75NGFR) in Hirschsprung's disease显示文摘TheclasicalexplanationoftheetiologyofHirschsprung’sdisease(HD)isthefailureofmigrationofneuralcrestcelsintothegutduringembryon... | 牟雪松 王夫 王惠忠 | 1999 | Chinese Medical Journal1999，，3： | 0 |
| 17 | Effects of Nerve Growth Factor on Excitatory Amino Acid Content in Spinal Cord Neuron after Spinal Cord Injury显示文摘IntroductionWeevaluatedtheefectofNGFfolowingspinalcordinjury(SCI)bydetectingthecontentofexcitatoryaminoacids(EAA),andtoexplor... | 曹晓建 罗永湘 | 1999 | The Journal of Biomedical Research1999，23，1： | 0 |
| 18 | CLONING AND SEQUENCING OF MATURED FRAGMENT OF HUMAN NEVER GROWTH FACTOR GENE显示文摘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. | 马巍 吴玲 王德利 刘淼 任惠民 杨广笑 王全颖 | 2003 | Journal of Pharmaceutical Analysis2003，15，1： | 0 |
| 19 | Nerve growth factor activity of several immunal related serine proteases显示文摘Rabbit was immuned by the previously purified protein with high nerve growth factor (NGF) bioactivity (NGF_like protease) from \%Agkistrodon halys Pallas\% and the antisera were collected. The polyclonal antibodies were tentatively purified and then used as ligands of an affinity column. The \%A.h.Pallas\% crude venom was fractionated by this affinity column and then by Mono Q on fast protein liquid chromatography (FPLC). As a result, fraction Ⅱ and fraction Ⅲ were purified respectively, whose N_terminal amino acid sequences show high homology with the serine proteases in snake venoms, as well as the previous NGF_like protease. However, they possessed different levels of NGF bioactivity. The NGF activity of the previous NGF_like protease is equivalent to that of NGF, while the activity of fraction Ⅱ seems relatively low in contrast to fraction Ⅲ which had no NGF activity. | Liying Guo Hong Zhu Yuancong Zhou | 1998 | Chinese Science Bulletin1998，43，22： | 0 |
| 20 | Effects of Nerve Growth Factor on Axonal Retrograde Transport after Axonal Injury of Motoneurons显示文摘(方煌)(罗永湘)EffectsofNerveGrowthFactoronAxonalRetrogradeTransportafterAxonalInjuryofMotoneuronsFANGHuang;LUOYongxiang(Department... | 方煌 罗永湘 | 1996 | Journal of Huazhong University of Science and Technology(Medical Sciences)1996，16，1： | 0 |
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