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Effect of hydroxysafflor yellow A(HSYA) on neuron against hypoxia/reoxygenation injury and its mechanism
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DOI   10.11656/j.issn.1672-1519.2023.11.20
Key Words   hydroxysafflor yellow A;neuron;hypoxia/reoxygenation;synaptic plasticity
Author NameAffiliationE-mail
JIA Xiaoxu Department of Pharmacy, Ordos Hospital of Traditional Chinese Medicine, Ordos 017010, China
Tianjin University of Traditional Chinese Medicine, Tianjin 301617, China 
 
ZHANG Yibo Tianjin University of Traditional Chinese Medicine, Tianjin 301617, China
State Key Laboratory of Component-Based Chinese Medicine, Institute of Traditional Chinese Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin 301617, China 
 
YUAN Qing Tianjin University of Traditional Chinese Medicine, Tianjin 301617, China
State Key Laboratory of Component-Based Chinese Medicine, Institute of Traditional Chinese Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin 301617, China 
 
WANG Shuo Tianjin University of Traditional Chinese Medicine, Tianjin 301617, China  
ZHU Jinqiang Tianjin University of Traditional Chinese Medicine, Tianjin 301617, China
State Key Laboratory of Component-Based Chinese Medicine, Institute of Traditional Chinese Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin 301617, China 
zhujinqiang1860@163.com 
Abstract
    [Objective] To introduce HSYA might act as a potential neuroprotective agent against the hypoxia/reoxygenation(H/R)injury in neuron. [Methods] Cortical neurons of Wistar rat were primary cultured in vitro. The cortical neurons were divided randomly into five groups:control, H/R and HSYA(5, 20, 80 μg/mL)+H/R. By observing the changes of cell viability and the releasing of LDH, proved the effect of HSYA on neuron injuried by H/R. The expressions of BDNF, GAP-43 and NogoA were studied. By using real-time RT-PCR and ELISA. [Results] Compared with control group, the cell viability decreased and the releasing of LDH increased significantly(P<0.01), the mRNA and protein expressions of BDNF and GAP-43 decreased significantly(P<0.05), the mRNA and protein expression of NogoA increased significantly(P<0.01) in H/R group. Compared with control group, three dosages of HSYA increased cell viability and reduced the releasing of LDH significantly(P<0.01), and increased the mRNA and protein expressions of BDNF and GAP-43, and decreased the mRNA and protein expressions of NogoA(P<0.05 or P<0.01). [Conclusion] HSYA could increase cell viability, and reduce the releasing of LDH, thus relieving the neuronal damage caused by H/R, which related to promoting BDNF expression. In addition, HSYA can also promote the neuronal synaptic plasticity by promoting the expression of GAP-43 mRNA and protein, and inhibiting the expression of Nogo-An mRNA and protein.

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