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HO-1 attenuates hippocampal neurons injury via the activation of BDNF-TrkB-PI3K/Akt signaling pathway in stroke 期刊论文

编号：

ed2f5d74-6fd7-4a93-b3e4-eaa4580fe718
作者：

Qi, Dashi^[1] Ouyang, Changjie^[2] Wang, Yulan^[2] Zhang, Shichun^[2] Ma, Xijuan^[4] Song, YuanJian^[1] Yu, HongLi^[1] Tang, Jiali^[5] Fu, Wei^[6] Sheng, Lei^[7] Yang, Lihua^[1] Wang, Mei^[1] Zhang, Weihao^[1] Miao, Lei^[1] Li, Tengteng^[1] Huang, Xiaojing^[3] Dong, Hongyan^[1,3]
语种：

English
期刊：

BRAIN RESEARCH ISSN：0006-8993 2014 年 1577 卷 (69 - 76) ; AUG 19
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关键词：

HO-1 Stroke Brain-derived neurotrophic factor (BNDF) TrkB PI3K/Akt Apoptosis
摘要：

Although recent studies have found that HO-1 plays an important role in neuronal survival, little is known about the precise mechanisms occurring during cerebral ischemia/reperfusion (I/R). Therefore, the aim of this study was to investigate the neuroprotective mechanisms of HO-1 against ischemic brain injury induced by cerebral I/R and to explore whether the BDNF-TrkB-PI3K/Akt signaling pathway contributed to the protection provided by HO-1. Over-expressed HO-1 plasmids were employed to induce the overexpression of HO-1 through hippocampi CA1 injection 5 days before the cerebral I/R animal model was induced by four-vessel occlusion for 15 min transient ischemia and followed by reperfusion in Sprague-Dawley rats. Immunoblotting was carried out to examine the expression of the related proteins, and HE-staining was used to detect the percentage of living neurons in the hippocampal CA1 region. The results showed that over-expressed HO-1 could significantly protect neurons against cerebral I/R. Furthermore, the protein expression of BDNF, TrkB and p-Akt also increased in the rats treated with over-expressed HO-1 plasmids. However, treatment with tropomyosin receptor kinase B (TrkB) receptor antagonist (K252a) reversed the HO-1-induced increase in BDNF and p-Akt protein levels and decreased the level of cleaved caspase-3 protein in I/R rats. In summary, our results imply that HO-1 can decrease cell apoptosis in the I/R rat brain and that the mechanism may be related to the activation of the BDNF-TrkB-PI3K/Akt signaling pathway. (C) 2014 Published by Elsevier B.V.
推荐引用方式
GB/T 7714：

Qi Dashi,Ouyang Changjie,Wang Yulan, et al. HO-1 attenuates hippocampal neurons injury via the activation of BDNF-TrkB-PI3K/Akt signaling pathway in stroke [J].BRAIN RESEARCH,2014,1577:69-76.
APA：

Qi Dashi,Ouyang Changjie,Wang Yulan,Zhang Shichun,&Dong Hongyan.(2014).HO-1 attenuates hippocampal neurons injury via the activation of BDNF-TrkB-PI3K/Akt signaling pathway in stroke .BRAIN RESEARCH,1577:69-76.
MLA：

Qi Dashi, et al. "HO-1 attenuates hippocampal neurons injury via the activation of BDNF-TrkB-PI3K/Akt signaling pathway in stroke" .BRAIN RESEARCH 1577(2014):69-76.

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