Yuli Liu

Liaoning Universtity of Traditional Chinese Medicine, Feng-t’ien, Liaoning, China

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Publications (6)12.16 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Nerve growth factor (NGF) is an important nerve cell growth regulatory factor and has an indispensable role in the development, survival and regeneration of the cholinergic basal forebrain (CBF) neurons, and it has multiple targets when used for Alzheimer’s Disease (AD) therapy. In this study, we observed whether NGF can affect cholinergic neurons to change amyloid-β precursor protein (APP) metabolism process and reduce amyloidosis in AD brains. NGF was administered intranasally to APP/PS1 double-transgenic mice for 14 weeks. We observed an increase in APP695 and ADAM10 and a decrease in BACE1 and PS1 protein levels and, subsequently, a reduction in Aβ1-40 and Aβ1-42 levels and Aβ burden were present in NGF-treated mice brains, suggesting that NGF enhanced the APP nonamyloidogenic cleavage pathway and reduced the Aβ generation in the APP/PS1 transgenic mice brains.
    Neuropeptides 01/2014; · 2.07 Impact Factor
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    ABSTRACT: Nerve growth factor (NGF), combined with the high‑affinity tyrosine kinase receptor A (TrkA), has been reported to be involved in the pathogenesis of asthma. Ankyrin‑rich membrane spanning/transmembrane substrate of protein kinase D (ARMS/Kidins220), a TrkA‑binding protein, modulates the NGF signaling pathway. The aim of the present study was to investigate the expression of Kidins220/ARMS and the effect NGF has on the protein in the spleen and peripheral blood, following airway allergen challenge in mice. BALB/c mice were sensitized and challenged with ovalbumin. The effects of NGF on Kidins220/ARMS in the spleen and peripheral blood of mice were assessed by administering anti-NGF antibody. Expression of ARMS, interleukin (IL)‑1β and IL‑4 in the spleen and peripheral blood was observed by reverse transcription‑polymerase chain reaction, western blot analysis and immunohistochemistry. Pathological changes in the bronchi and lung tissues were examined by hematoxylin and eosin staining. Results showed that Kidins220/ARMS, IL‑1β and IL‑4 were overexpressed in the spleen and peripheral blood following allergen challenge, compared with the control mice. Moreover, following treatment with anti-NGF, the levels of Kidins220/ARMS, IL‑1β and IL‑4 in the mice were downregulated. Therefore, the results of the present study showed that Kidins220/ARMS is expressed in the spleen and peripheral blood of normal BALB/c mice and may participate in the immuno‑inflammation of asthma through the NGF‑mediated signaling pathway.
    Molecular Medicine Reports 10/2013; · 1.17 Impact Factor
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    ABSTRACT: BALB/c mice were sensitized and challenged with ovalbumin. We hypothesized that Kidins220/ARMS influences airway inflammation and hyper-responsiveness during allergic airway challenge, and assessed it by intranasal administration of anti-NGF antibody or anti-ARMS antibody to mice. Airway resistance was measured using a sealed whole-body plethysmograph. Total cell numbers and the percentage of different inflammatory cells in BALF were counted. Expression of IL-1β, IL-4 and TNF-α were determined by ELISA, and NF-κB activation determined by EMSA. Kidins220/ARMS expression was observed in ovalbumin-sensitized mice by immunofluorescence or western blotting. IL-1β, IL-4, and TNF-α were overexpressed and NF-κB activation increased after allergen challenge compared with controls. After treatment with anti-ARMS or anti-NGF, levels of IL-1β, IL-4 and TNF-α and NF-κB activation were reduced in comparison with those of ovalbumin-sensitized mice. These results suggest that NGF-mediated Kidins220/ARMS signaling participates in the pathogenesis of asthma, and contributes to airway inflammation and hyper-responsiveness in ovalbumin-sensitized mice.
    Respiratory Physiology & Neurobiology 01/2011; 175(1):97-103. · 2.05 Impact Factor
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    ABSTRACT: Nerve growth factor (NGF) contributes to airway inflammation and bronchoconstriction in allergic asthma. The Src homology 2beta/serine/threonine kinase (SH2-Bbeta/Akt) pathway is one of the avenues through which NGF regulates the biological activity of pheochromocytoma (PC)12 cells. It has also been reported that NGF upregulates the expression of SH2-Bbeta in the lung tissue of asthmatic mice. The present study investigated the effects of NGF and SH2-Bbeta on Akt activation during allergic airway challenge. BALB/c mice were sensitized and challenged with ovalbumin. The effects of NGF and SH2-Bbeta on Akt in allergic airway challenge were assessed by intravenously administering anti-NGF antibody or a mutant of SH2-Bbeta (R555E) to these mice. Pulmonary histological changes were then assessed and the inflammatory cells in the BAL fluid (BALF) were counted. Additionally, phosphorylated Akt (p-Akt) expression was determined by fluorescence microscopy, western blotting and quantitative RT-PCR. Airway resistance was also measured using closed-type body plethysmography. We observed p-Akt overexpression in the lungs after allergen challenge by fluorescence microscopy, Western blotting and RT-PCR, as compared with the control. However, after treatment with anti-NGF or R555E, p-Akt levels and allergen-induced airway inflammation were reduced in comparison with those of allergen-challenged mice. Anti-NGF and R555E also decreased airway hyperresponsiveness caused by allergen challenge in response to methacholine (MCH). These results suggest that SH2-Bbeta regulation of Akt partly participates in the NGF-mediated development of allergic airway challenge.
    Respirology 11/2009; 15(1):80-7. · 2.78 Impact Factor
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    ABSTRACT: The Toll-like receptor 4 (TLR4)-mediated myeloid differentiation factor 88 (MyD88)-dependent signaling pathway plays an essential role in inflammation resulting from invading microbes. However, whether the signaling pathway is activated in the inflammatory reaction of cerebral ischemia-reperfusion and its mechanism is still unclear. In this experiment mice were randomly divided into sham group, ischemia/reperfusion group and TLR4-blocked group with different time points of reperfusion at 12, 24, 48 and 72 h . Mice cerebral ischemia was induced by occlusion of common carotid arteries (CCA) bilaterally. TLR4 signaling pathway was inhibited using specific anti-TLR4 binding protein to prevent TLR4 from interacting with its receptors. We determined the result of TLR4 antibodies-blocking and mice cerebral ischemia-reperfusion injuries by Western blot, and evaluated neuronal damage in the hippocampus. We also determined expression of TLR4 mRNA and MyD88 mRNA by in situ hybridization (ISH), activation of nuclear factor (NF)-kappaB by electrophoretic mobility-shift analysis (EMSA), and expression of interrleukin (IL)-1beta protein by Western blot. The results demonstrated that TLR4-mediated MyD88-dependent signaling pathway activated by ischemia-reperfusion may be involved in the mechanism of ischemia-reperfusion through upregulation of NF-kappaB, IL-1beta.
    Biological & Pharmaceutical Bulletin 10/2009; 32(10):1665-71. · 1.85 Impact Factor
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    ABSTRACT: To study whether the signaling pathway is activated in the inflammatory reaction of cerebral ischemia-reperfusion and its mechanism. The mice were randomly divided into sham group, ischemia-reperfusion group and TLR4-blocked group with different time points of reperfusion 12h, 24h, 48h and 72h group. We observed the different expression of TLR4 mRNA and MyD88 mRNA, activation of NF-kappaB and the TNF-alpha and IL-1beta protein levels in each group at different time point after ischemia-reperfusion. Mice cerebral ischemia was induced by occlusion of common carotid arteries (CCA) bilaterally. TLR4 signaling pathway could be inhibited by specific anti-TLR4 binding protein to prevent TLR4 from interacting with its receptors. We determined the result of TLR4 antibodies-blocking and mice cerebral ischemia-reperfusion injuries by Western blot, and evaluated neuronal damage in cortex. We also determined the expression of TLR4 mRNA and MyD88 mRNA by in situ hybridization (ISH), the activation of NF-kappaB by EMSA, and the expression of TNF-alpha protein by Western blot. Anti-TLR4 binding TLR4 receptors before reperfusion was effective; There was distinct difference among each group respecting neuronal damage; The expression of TLR4 mRNA and MyD88 mRNA, the activation of NF-kappaB, and the expression of TNF-alpha protein showed clear difference as well. LR4-mediated MyD88-dependent signaling pathway activated by ischemia-reperfusion may be involved in the mechanism of ischemia-reperfusion through upregulation of NF-kappaB and TNF-alpha.
    Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 08/2008; 63(6):442-50. · 2.24 Impact Factor

Publication Stats

27 Citations
12.16 Total Impact Points

Institutions

  • 2014
    • Liaoning Universtity of Traditional Chinese Medicine
      Feng-t’ien, Liaoning, China
  • 2009–2011
    • China Medical University (PRC)
      • Department of Neurobiology
      Shenyang, Liaoning, China