Liang Zhou

Peking University Third Hospital, Peping, Beijing, China

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Publications (8)38.71 Total impact

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    ABSTRACT: Amyloid-β (Aβ) peptide, which can invoke a cascade of inflammatory responses, is considered to play a causal role in the development and progress of Alzheimer's disease (AD). Xylocoside G (XG) is an active compound isolated from a traditional Chinese medicinal plant, Itoa orientalis. We have previously reported that XG has neuroprotective effects, of which the mechanism is yet unknown. In this study, we investigated the possible mechanisms underlying neuroprotection of XG against Aβ-induced toxicity in SH-SY5Y cells and primary neurons. Pretreatment with XG significantly attenuated the cell viability reduction induced by Aβ exposure in a dose dependent manner which was testified by 3-[4,5-Dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT) and lactate dehydrogenase release assay. In addition, pretreatment with XG countered the effect of Aβ on Bax and Bcl-2 expression and repressed Aβ-induced caspase-3 activation, suggesting that the neuroprotective effect of XG is associated with apoptosis regulation. Neuroinflammation has been implicated in Aβ-induced neuronal death. XG significantly attenuated Aβ-stimulated release of inflammatory factors such as tumor necrosis factor-α, interleukin-1β, and prostaglandin E2. It also downregulated the expression of cyclooxygenase-2 in SH-SY5Y cells. Further molecular mechanism studies demonstrated that XG inhibited Aβ-induced NF-κB p65 translocation, which was probably the result of inhibition of JNK phosphorylation but not ERK or p38 MAPK pathway by XG. This is the first study to demonstrate that XG protects SH-SY5Y cells against Aβ-induced inflammation and apoptosis by down-regulating NF-κB signaling pathways.
    Journal of Alzheimer's disease: JAD 03/2012; 30(2):263-75. DOI:10.3233/JAD-2012-110779 · 4.15 Impact Factor
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    Molecular Neurodegeneration 02/2012; 7 Suppl 1(Suppl 1):O9. DOI:10.1186/1750-1326-7-S1-O9 · 6.56 Impact Factor
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    Molecular Neurodegeneration 02/2012; 7 Suppl 1(Suppl 1):S27. DOI:10.1186/1750-1326-7-S1-S27 · 6.56 Impact Factor
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    Molecular Neurodegeneration 02/2012; 7 Suppl 1(Suppl 1):S28. DOI:10.1186/1750-1326-7-S1-S28 · 6.56 Impact Factor
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    Molecular Neurodegeneration 02/2012; 7 Suppl 1(Suppl 1):O10. DOI:10.1186/1750-1326-7-S1-O10 · 6.56 Impact Factor
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    ABSTRACT: Formononetin, an active constituent of the Chinese herb Astragali Radix, has been reported to have beneficial effects for Alzheimer's disease (AD). Yet the mechanism of this effect remains to be elucidated. The present study shows that formononetin increases soluble-AβPPα (sAβPPα) secretion and thus protects human-AβPP Swedish mutation cell (N2a-AβPP cell) from hypoxia-induced apoptosis. Using hypoxic N2a-AβPP cell as an in vitro model of AD-like pathology, we confirmed that regular treatment with formononetin could have neuroprotective effects, followed respectively by reduced caspase 3 activity and increased cell viability. Strikingly, our data revealed that the caspase 3-blocking effect of formononetin was largely mediated by stimulation of α-secretase cleavage of AβPP, and increasing the secretion of its soluble form, sAβPPα. Moreover, the protective effect of formononetin was totally inhibited by TAPI-2, an α-secretase complex inhibitor, suggesting the role of the sAβPPα pathway in the neuroprotective response to formononetin. We also found that the stimulative effect of formononetin on α-secretase activity was mainly conducted by upregulating ADAM10 expression at the transcriptional level. Altogether, our study provides novel insights into how formononetin mediates stimulation of the ADAM10-sAβPPα pathway and exerts a neuronal protective effect.
    Journal of Alzheimer's disease: JAD 11/2011; 28(4):795-808. DOI:10.3233/JAD-2011-110506 · 4.15 Impact Factor
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    ABSTRACT: Alzheimer's disease (AD), the most common form of dementia, is characterized by the presence of excessive deposits of aggregated amyloid-beta (Abeta), which is derived from the amyloid-beta protein precursor (AbetaPP) following processing by beta- and gamma-secretase. Metal elements are implicated in the pathophysiology of AD. Magnesium affects many biochemical mechanisms vital for neuronal properties and synaptic plasticity, and magnesium levels were reported to be decreased in various tissues including brain of AD patients. However, the exact role of magnesium in the neurodegenerative process of AD remains elusive. In this study, we investigated the effects of physiological (0.8 mM, as normal control), low (0-0.4 mM), and high (1.2-4.0 mM) concentrations of extracellular magnesium ([Mg2+]o) on AbetaPP processing and Abeta secretion. Here we show the effects of varying [Mg2+]o on AbetaPP processing is time- and dose-dependent. After 24 h treatment, high [Mg2+]o increased C-terminal fragment-alpha (CTFalpha) levels and soluble alpha-secretase cleaved AbetaPP (sAbetaPPalpha) release via enhancing retention of AbetaPP on plasma membrane. In contrast, low [Mg2+]o enhanced CTFbeta accumulation and Abeta secretion, and reduced cell surface AbetaPP level. Varying [Mg2+]o did not alter protein contents of full length AbetaPP. However, decreased total intracellular magnesium level by magnesium deprivation over 24 hr impaired cell viability. Normal AbetaPP processing could be restored when magnesium was adjusted back to physiological concentration. These data demonstrate that AbetaPP processing can be modulated by magnesium and at high [Mg2+]o, AbetaPP processing favors the alpha-secretase cleavage pathway. Our findings suggest that supplementation of magnesium has a therapeutic potential for preventing AD.
    Journal of Alzheimer's disease: JAD 04/2010; 20(4):1091-106. DOI:10.3233/JAD-2010-091444 · 4.15 Impact Factor
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    ABSTRACT: Several varieties oflentiviral delivery systems have been used to generate stable cell lines and transgenic animals. Some enhancing elements have been identified to promote stable transgene expression. In this study, we describe that the promoter activity is affected by the lentiviral genomic context. We have examined the promoter activities using green fluorescence protein (GFP) as a reporter in different cell lines to demonstrate that the cytomegalovirus (CMV) promoter may not always be the best choice to overexpress transgenes in all cell types. Our data showed that the polypeptide chain elongation factor 1 alpha (EF1alpha) promoter is relatively active in all three model cell lines (293T, HOS, and Hela) while the CMV promoter is less effective in Hela cells.
    Acta bio-medica: Atenei Parmensis 01/2009; 79(3):192-6.

Publication Stats

49 Citations
38.71 Total Impact Points


  • 2012
    • Peking University Third Hospital
      Peping, Beijing, China
  • 2010–2012
    • Peking University
      Peping, Beijing, China
  • 2009
    • Logistical College of Chinese People's Armed Police Force
      T’ien-ching-shih, Tianjin Shi, China