Xiao-Yuan Zhao

Soochow University (PRC), Suzhou, Jiangsu Sheng, China

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Publications (3)6.49 Total impact

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    ABSTRACT: Matrine (Mat) and oxymatrine are two major alkaloids of the Chinese herb Sophora flavescens Ait. (Leguminosae). Previous study has demonstrated that Mat reduces brain edema induced by focal cerebral ischemia. More recently, oxymatrine has been reported to produce neuroprotective effects against focal cerebral ischemia via inhibiting the activation of NF-κB in the ischemic brain tissue. In the current study, we investigated whether direct protection on neurons and astrocytes via inhibition of NF-κB signaling pathway is associated with Mat's neuroprotective effects against cerebral ischemia. In a model of permanent middle cerebral artery occlusion (pMCAO), Mat (12.5, 25 and 50 mg/kg) reduced the infarction volume and improved the neurological deficits in a dose-dependent manner, administered 10 min, 3h and even 6h following pMCAO. Mat 50 mg/kg also decreased the hemispheric water content. The number of GFAP-positive cells was markedly decreased in the ischemic cortex at 12h after ischemia. In contrast, Mat increased the number of GFAP-positive cells. Mat 50mg/kg has no effect on the cerebral blood flow (CBF). Primary neuron or astrocyte cultures were exposed to a paradigm of ischemic insult by using an oxygen-glucose deprivation (OGD), Mat (50-200 μM) reduced LDH leakage and the number of neuronal and astrocytic apoptosis, and increased the number of MAP2-positive and GFAP-positive cells. Further observations revealed that Mat increased the protein levels of IκBα, and blocked the translocation of NF-κB p65 from the cytosol to the nucleus in the ischemic cortex and injured neurons and astrocytes induced by in vitro OGD. Moreover, Mat could down-regulate NF-κB p65 downstream pro-apoptotic gene p53 and/or c-Myc in the injured neurons and astrocytes induced by OGD. The present findings suggest that Mat, even when administrated 6h after ischemia, has neuroprotective effects against focal cerebral ischemia and directly protects neurons and astrocytes via inhibition of NF-κB signaling pathway, contributing to matrine's neuroprotection against focal cerebral ischemia.
    Brain research 03/2012; 1454:48-64. DOI:10.1016/j.brainres.2012.03.020 · 2.83 Impact Factor
  • Li-Zhi Hong, Xiao-Yuan Zhao, Hui-Ling Zhang
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    ABSTRACT: p53 is a key modulator of cellular stress responses. It is activated in the ischemic areas of brain, and contributes to neuronal apoptosis. In various stroke models, p53 deficiency or applications of p53 inhibitors can significantly attenuate brain damage. p53-mediated neuronal apoptosis occurs through various molecular mechanisms. The transcriptional pathway is an important mechanism through which p53 induces neuronal apoptosis by up-regulating the expression of its target gene p21(WAF), Peg3/Pw1 or p53-up-regulated modulator of apoptosis (PUMA). In addition, p53 disrupts NF-kappaB binding to p300 and blocks NF-kappaB-mediated survival signaling. On the other hand, the transcription-independent pathway mechanism is also of great importance. In this pathway, p53 is translocated to mitochondrial and mediates the release of cytochrome c. In both pathways, p53 seems to play a key role in post-ischemic brain damage and has become a therapeutic target against stroke pathology.
    Neuroscience Bulletin 06/2010; 26(3):232-40. DOI:10.1007/s12264-010-1111-0 · 1.83 Impact Factor
  • Li-Zhi Hong, Xiao-Yuan Zhao, Hui-Ling Zhang
    Neuroscience Bulletin 01/2010; 26(3):232-240. · 1.83 Impact Factor

Publication Stats

40 Citations
6.49 Total Impact Points

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Institutions

  • 2010–2012
    • Soochow University (PRC)
      • Department of Pharmacology
      Suzhou, Jiangsu Sheng, China