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Neuroprotection via maintenance or increase of antioxidants and neurotrophic factors in ischemic gerbil hippocampus treated with tanshinone Ⅰ

摘要Background Danshen (Radix Salvia miltiorrhizae) has been used as a traditional medicine in Asia for treatment of various microcirculatory disturbance related diseases.Tanshinones are mainly hydrophobic active components,which have been isolated from Danshen and show various biological functions.In this study,we observed the neuroprotective effect of tanshinone Ⅰ (Tsl) against ischemic damage in the gerbil hippocampal CA1 region (CA1) after transient cerebral ischemia and examined its neuroprotective mechanism.Methods The gerbils were divided into vehicle-treated-sham-group,vehicle-treated-ischemia-group,Tsl-treated-shamgroup,and Tsl-treated-ischemia-group.Tsl was administrated intraperitoneally three times (once a day for three days) before ischemia-reperfusion.The neuroprotective effect of Tsl was examined using H&E staining,neuronal nuclei (NeuN) immunohistochemistry and Fluoro-Jade B staining.To investigate the neuroprotective mechanism of Tsl after ischemiareperfusion,immunohistochemical (IHC) and Western blotting analyses for Cu,Zn-superoxide dismutase (SOD1),Mnsuperoxide dismutase (SOD2),brain-derived neurotrophic factor (BDNF) and insulin-like growth factor-I (IGF-I) were performed.Results Treatment with Tsl protected pyramidal neurons from ischemia-induced neuronal death in the CA1 after ischemia-reperfusion.In addition,treatment with Tsl maintained the levels of SOD1 and SOD2 as determined by IHC and Western blotting in the CA1 after ischemiareperfusion compared with the vehicle-ischemia-group.In addition,treatment with Tsl increased the levels of BDNF and IGF-I determined by IHC and Western blotting in the Tsl-treated-sham-group compared with the vehicle-treatedsham-group,and their levels were maintained in thestratum pyramidale of the ischemic CA1 in the Tsl-treatedischemia-group.Conclusion Treatment with Tsl protects pyramidal neurons of the CA1 from ischemic damage induced by transient cerebral ischemia via the maintenance of antioxidants and the increase of neurotrophic factors.

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作者单位 Department of Neurobiology, School of Medicine, Kangwon National University, Chuncheon 200-701, South Korea [1] Division of Analytical Bio-Imaging, Chuncheon Center, Korea Basic Science Institute, Chuncheon 200-701, South Korea [2] Department of Integrative Traditional & Western Medicine, Medical College, Yangzhou University, Yangzhou, Jiangsu 225001, China [3]
栏目名称 ORIGINAL ARTICLES
DOI 10.3760/cma.j.issn.0366-6999.20140818
发布时间 2014-10-28
基金项目
This research was supported by Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education,Science and Technology by 2013 Research Grant from Kangwon National University
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中华医学杂志(英文版)

中华医学杂志(英文版)

2014年127卷19期

3396-3405页

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