Heng-Tong Fang

Academy of Military Medical Sciences, T’ien-ching-shih, Tianjin Shi, China

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Publications (2)3.29 Total impact

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    ABSTRACT: An experiment was performed to observe changes of mitogen-activated protein kinase ERK (MEK)/extracellular signal-regulated kinase (ERK) signaling pathways in the hippocampus of zinc-deficient (ZD) rats and the correlation with cognitive dysfunction. Forty-four male weanling Wistar rats were randomly assigned to ZD (n = 22) and control (pair-fed, n = 22) groups. After a 4-week treatment, Y-maze was used to test the spatial memory of the rats. The long-term potentiation (LTP) in rat hippocampal dentate gyrus was observed simultaneously. pMEK, pERK1/2, and pCREB protein levels were examined by Western blot assays. The results demonstrated that the latency period in Y-maze was significantly shorter for the ZD rats. LTP amplitude in the ZD group decreased significantly compared with the control group. pMEK, pERK1/2, and pCREB protein expression of hippocampus in the ZD group decreased significantly. The results implicated a possibility that zinc deficiency-induced cognitive and synaptic impairment may be relevant to the MEK/ERK signaling pathway.
    Nutritional Neuroscience 03/2011; 14(2):45-50. · 1.65 Impact Factor
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    ABSTRACT: Zinc deficiency has been associated with impaired learning and memory function in animals and human beings. However, the molecular mechanisms remain obscure. In light of evidence that ubiquitin C-terminal hydrolase L1 (Uch-L1) and cAMP-responsive element-binding protein (CREB) are required for synaptic and memory function and the possible regulation of CREB by Uch-L1, this present study was conducted to investigate the effect of zinc depletion on Uch-L1 protein expression and on Uch-L1 and CREB mRNA expression in cultured hippocampal neurons. Cultured hippocampal neurons were exposed to a cell membrane-permeant zinc chelator TPEN (2 microM), and to TPEN plus zinc sulphate (5 microM) for 24 h. Cultures were then processed to detect neuronal injury by lactate dehydrogenase (LDH) assay, Uch-L1 protein levels by Western blot, and Uch-L1 and CREB mRNAs levels by RT-PCR. The LDH release rate in TPEN-incubated neurons was notably increased compared to non-treated controls. Significant down-regulation of Uch-L1 protein level and mRNA levels for Uch-L1 and CREB were observed in TPEN-treated neurons. Co-addition of zinc almost completely reversed TPEN-induced neuronal injury and the alterations in Uch-L1 and CREB expression. The results demonstrated that zinc modulated the expression of Uch-L1 and CREB at the protein and/or transcription levels in hippocampal neurons, which implies that down-regulation of both Uch-L1 and CREB might participate in memory dysfunction induced by zinc deficiency.
    Nutritional Neuroscience 07/2008; 11(3):96-102. · 1.65 Impact Factor

Publication Stats

5 Citations
3.29 Total Impact Points

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Institutions

  • 2011
    • Academy of Military Medical Sciences
      T’ien-ching-shih, Tianjin Shi, China