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  • Up-regulation of neurotrophic factors by cinnamon and its metabolite sodium benzoate: therapeutic implications for neurodegenerative disorders. 23475543

    This study underlines the importance of cinnamon, a widely-used food spice and flavoring material, and its metabolite sodium benzoate (NaB), a widely-used food preservative and a FDA-approved drug against urea cycle disorders in humans, in increasing the levels of neurotrophic factors [e.g., brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3)] in the CNS. NaB, but not sodium formate (NaFO), dose-dependently induced the expression of BDNF and NT-3 in primary human neurons and astrocytes. Interestingly, oral administration of ground cinnamon increased the level of NaB in serum and brain and upregulated the levels of these neurotrophic factors in vivo in mouse CNS. Accordingly, oral feeding of NaB, but not NaFO, also increased the level of these neurotrophic factors in vivo in the CNS of mice. NaB induced the activation of protein kinase A (PKA), but not protein kinase C (PKC), and H-89, an inhibitor of PKA, abrogated NaB-induced increase in neurotrophic factors. Furthermore, activation of cAMP response element binding (CREB) protein, but not NF-κB, by NaB, abrogation of NaB-induced expression of neurotrophic factors by siRNA knockdown of CREB and the recruitment of CREB and CREB-binding protein to the BDNF promoter by NaB suggest that NaB exerts its neurotrophic effect through the activation of CREB. Accordingly, cinnamon feeding also increased the activity of PKA and the level of phospho-CREB in vivo in the CNS. These results highlight a novel neutrophic property of cinnamon and its metabolite NaB via PKA - CREB pathway, which may be of benefit for various neurodegenerative disorders.
    Document Type:
    Reference
    Product Catalog Number:
    17-371
    Product Catalog Name:
    EZ-ChIP™

  • Involvement of neurotrophic factors in aging of noradrenergic innervations in hippocampus and frontal cortex. 16448713

    In the present study, we investigated the age-dependent changes in the axon terminals of the locus coeruleus (LC) neurons in the frontal cortex and hippocampus, in which a high degree of axonal branching in the middle-aged brain was suggested to occur in our previous electrophysiological study. We used 6-, 13- and 25-month-old male F344/N rats, and performed Western blot analysis of the norepinephrine transporter (NET), brain-derived neurotrophic factor (BDNF) and glial cell line-derived neurotrophic factor (GDNF). NET expression level increased in the 13-month-old hippocampus, but was not altered by aging in the frontal cortex. BDNF expression level increased in the hippocampus, but did not change with age in the frontal cortex. On the other hand, GDNF expression level was increased with age in the frontal cortex, but was not in the hippocampus. These results suggest that the LC noradrenergic innervations may be locally regulated by different neurotrophic factors that exert their trophic actions at different target sites.
    Document Type:
    Reference
    Product Catalog Number:
    MAB308
    Product Catalog Name:
    Anti-Dopamine β Hydroxylase Antibody, clone 4F10.2

  • Postnatal expression of neurotrophic factors accessible to spiral ganglion neurons in the auditory system of adult hearing and deafened rats. 25253857

    Spiral ganglion neurons (SGNs) receive input from cochlear hair cells and project from the cochlea to the cochlear nucleus. After destruction of hair cells with aminoglycoside antibiotics or noise, SGNs gradually die. It has been assumed that SGN death is attributable to loss of neurotrophic factors (NTFs) derived from hair cells or supporting cells in the organ of Corti (OC). We used quantitative PCR (qPCR) to assay NTF expression-neurotrophin-3 (NT-3), BDNF, GDNF, neurturin, artemin, and CNTF-in the OC and cochlear nucleus at various ages from postnatal day 0 (P0) to P90 in control hearing and neonatally deafened rats. NT-3, neurturin, and CNTF were most abundant in the postnatal hearing OC; CNTF and neurturin most abundant in the cochlear nucleus. In the OC, NT-3 and CNTF showed a postnatal increase in expression approximately concomitant with hearing onset. In rats deafened by daily kanamycin injections (from P8 to P16), surviving inner hair cells were evident at P16 but absent by P19, with most postsynaptic boutons lost before P16. NT-3 and CNTF, which normally increase postnatally, had significantly reduced expression in the OC of deafened rats, although CNTF was expressed throughout the time that SGNs were dying. In contrast, neurturin expression was constant, unaffected by deafening or by age. CNTF and neurturin expression in the cochlear nucleus was unaffected by deafening or age. Thus, NTFs other than NT-3 are available to SGNs even as they are dying after deafening, apparently conflicting with the hypothesis that SGN death is attributable to lack of NTFs.
    Document Type:
    Reference
    Product Catalog Number:
    Multiple
    Product Catalog Name:
    Multiple

  • Neuronal loss and expression of neurotrophic factors in a model of rat chronic compressive spinal cord injury. 16915089

    STUDY DESIGN: An experimental animal study about neuronal loss and the expression of neurotrophic factors in the chronic compressive spinal cords. OBJECTIVES: To investigate neuronal loss and the expression of neurotrophic factors in the chronic compressive spinal cords of rats, and to evaluate effects of decompressive procedures for the neuronal loss. SUMMARY OF BACKGROUND DATA: Chronic compression of spinal cords induces the loss of motor neurons in the anterior horn. However, the precise mechanism of this neuronal loss is not still understood completely. Furthermore, it is uncertain whether decompressive procedures prevent this neuronal loss or not. METHODS: A thin expanding polymer sheet was implanted microsurgically underneath T7 laminae of rats. After 6, 9, 12, and 15 weeks, the thoracic spinal cord was harvested and examined histopathologically. The expression of neurotrophic factors, including NGF, BDNF, NT-3, GDNF, CNTF, and VEGF, was analyzed using semiquantitative RT-PCR, enzyme immunoassay, and immunohistochemistry. Decompressive surgery was performed through the removal of T7 laminae and the compression materials 6, 9, and 12 weeks after starting compression. Three weeks later, respectively, the neuronal loss in the anterior horn was estimated. RESULTS: The spinal cords were progressively flattened by the expanding of the implanted polymer sheet, and the number of motor neurons in the anterior horn decreased, especially from 6 to 9 weeks after starting compression. Semiquantitative RT-PCR analysis showed that the expression of NGF and BDNF mRNAs was decreased significantly in the spinal cords of 12-week compression group compared with the 6-week compression group and that NGF mRNA expression was up-regulated significantly in the 6-week compression group relative to the 6-week control group. Any changes of expression of other neurotrophic factors were not significant. Since BDNF, not NGF, has been known to be one of the powerful survival factors for spinal motoneurons, we investigated the levels of BDNF protein in the compressive spinal cords using enzyme immunoassay and immunohistochemistry. We demonstrated the level of BDNF protein in the compressive spinal cords was increased 6 weeks after compression but declined after 12 weeks. The decompressive procedure in the 6 weeks after compression prevented neuronal loss, but the same procedure in the 9 or 12 weeks was ineffective. CONCLUSIONS: From the point of view of neuronal loss, decompressive surgery at an earlier stage, when compensatory mechanisms including the up-regulation of BDNF might be still effective, could provide better therapeutic results against chronic mechanical compressive spinal cord lesions.
    Document Type:
    Reference
    Product Catalog Number:
    AB1534
    Product Catalog Name:
    Anti-Brain Derived Neurotrophic Factor Antibody

  • Nanoporous peptide particles for encapsulating and releasing neurotrophic factors in an animal model of neurodegeneration. 22610659

    Neurotrophin-BDNF can be effectively encapsulated in nanoporous poly(L-glutamic acid) particles prepared via mesoporous silica templating. The loaded BDNF can be released in a sustained manner with retained biological activity. Animal experiments demonstrate the released BDNF can efficiently rescue the auditory neurons (as indicated by the arrows) in the cochlea of guinea pigs with sensorineural hearing loss.
    Document Type:
    Reference
    Product Catalog Number:
    S7100
    Product Catalog Name:
    ApopTag® Peroxidase In Situ Apoptosis Detection Kit

  • Human umbilical mesenchymal stem cells enhance the expression of neurotrophic factors and protect ataxic mice. 21683345

    Cerebellar ataxias, which comprise a wide spectrum of progressive disorders, are incurable at present. It has been reported that human umbilical mesenchymal stem cell (HU-MSC) transplantation has a protective effect on neurodegenerative diseases. In this study, we investigated the effect of HU-MSCs on ataxic mice induced by cytosine beta-D-arabinofuranoside (Ara-C). The ataxic mouse received an intravenous injection of 2×10(6) HU-MSCs once a week for three consecutive weeks. Neurological function was scored weekly by rotarod test and open field test. The mouse cerebellar volume and weight were also measured. The apoptotic cells, pathological alternations and distribution of HU-MSCs were determined by TUNEL assay and immunohistochemistry staining respectively. Double immunostaining was carried out to investigate the dynamics of HU-MSCs in the host animals. Neurotrophic factors in cerebellar tissue and serum were measured by Q-PCR and ELISA. Our results showed that HU-MSCs implantation significantly improved the motor skills of ataxic mice 8 weeks after application. HU-MSCs also alleviated cerebellar atrophy and decreased the number of apoptotic cells in the therapeutic group. Implanted HU-MSCs stayed in cerebellum for at least three months with no obvious differentiation. HU-MSC treated mice had enhanced expression of insulin-like growth factor-1 (IGF-1) and vascular endothelial growth factor (VEGF) in cerebellum extraction and blood serum. Double immunostaining revealed that a few MAB1287 positive cells co-localized with IGF-1 or VEGF express cells. Our results suggest that HU-MSC treatment is capable of alleviating the motor impairments and cerebellar atrophy in the ataxic mouse model, probably via promoting particular neurotrophic factors.
    Document Type:
    Reference
    Product Catalog Number:
    MAB1287

  • Therapeutic effects of human mesenchymal stem cells on traumatic brain injury in rats: secretion of neurotrophic factors and inhibition of apoptosis. 19508155

    To investigate the therapeutic effects and mechanisms of action of human mesenchymal stem cells (hMSCs), rats were intravenously treated with hMSCs 24 h after traumatic brain injury (TBI). Neurological function was significantly recovered in the hMSC-treated group by 15 days after TBI compared to the placebo group treated with saline. Quantitative ELISA of extracts from the entire traumatized cerebral hemispheres showed significantly increased expression of nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), and neurotrophin-3 (NT-3) in the hMSC group at 2 days after TBI, with expression decreasing over time. Western blot analysis demonstrated that pAkt expression was upregulated at 2 days after TBI, and caspase-3 cleavage was significantly decreased at 8 days after TBI in the hMSC group. Our results show that treatment of TBI with hMSCs during the acute phase of injury can enhance neurological functional outcome, and suggest that increased levels of neurotrophic factors in the injured hemisphere leading to decreased neuronal apoptosis is one mechanism by which functional recovery may occur.
    Document Type:
    Reference
    Product Catalog Number:
    MAB1281
    Product Catalog Name:
    Anti-Nuclei Antibody, clone 235-1

  • Neuroprotection associated with running: is it a result of increased endogenous neurotrophic factors? 12699770

    The possible neuroprotective effect of physical exercise was investigated in rats after middle cerebral artery occlusion (MCAO), a focal stroke model. It was found that physical exercise in the form of a 12-week treadmill running programme reduced the volume of infarction caused by MCAO. At the molecular level, reverse transcription polymerase chain reaction revealed that the runner had increased gene expression for nerve growth factor (NGF) over the nonrunner with or without MCAO. Expression of the NGF receptors, p75, was increased only in the absence of MCAO. In addition, runners showed a significantly higher number of cholinergic neurons, which constitutively expressed p75, in the horizontal diagonal band of Broca. The present findings suggest that neuroprotection after physical exercise may be a result of an increase in an endogenous neurotrophic factor nerve growth factor and the proliferation of its receptive cholinergic neurons.
    Document Type:
    Reference
    Product Catalog Number:
    MAB365
    Product Catalog Name:
    Anti-Nerve Growth Factor Receptor Antibody, extracellular, clone 192-IgG