机构:[1]Department of Neurosurgery, Stanford University School of Medicine, Stanford, California, USA[2]Department of Neurosurgery, Huashan Hospital, Fudan University, Shanghai, China[3]Department of Neurosurgery, Shanghai Jingan District Central Hospital, Shanghai, China[4]Department of Neurosurgery, Xuanwu Hospital, Capital Medical University, Beijing, China神经外科首都医科大学宣武医院[5]Stanford Stroke Center, Stanford University School of Medicine, Stanford, California, USA
While pre-conditioning is induced before stroke onset, ischemic post-conditioning (IPostC) is performed after reperfusion, which typically refers to a series of mechanical interruption of blood reperfusion after stroke. IPostC is known to reduce infarction in wild-type animals. We investigated if IPostC protects against brain injury induced by focal ischemia in Tcell-deficient nude rats and to examine its effects on Akt and the mammalian target of rapamycin (mTOR) pathway. Although IPostC reduced infarct size at 2days post-stroke in wild-type rats, it did not attenuate infarction in nude rats. Despite the unaltered infarct size in nude rats, IPostC increased levels of phosphorylated Akt (p-Akt) and Akt isoforms (Akt1, Akt2, Akt3), and p-mTOR, p-S6K and p-4EBP1 in the mTOR pathway, as well as growth associated Protein 43 (GAP43), both in the peri-infarct area and core, 24h after stroke. IPostC improved neurological function in nude rats 1-30days after stroke and reduced the extent of brain damage 30days after stroke. The mTOR inhibitor rapamycin abolished the long-term protective effects of IPostC. We determined that IPostC did not inhibit acute infarction in nude rats but did provide long-term protection by enhancing Akt and mTOR activity during the acute post-stroke phase.
基金:
AHA (Western State Affiliate) grant in aid (10GRNT4200024 )
NIH grant (1R01NS 064136 )
第一作者机构:[1]Department of Neurosurgery, Stanford University School of Medicine, Stanford, California, USA[2]Department of Neurosurgery, Huashan Hospital, Fudan University, Shanghai, China[3]Department of Neurosurgery, Shanghai Jingan District Central Hospital, Shanghai, China
通讯作者:
通讯机构:[*1]Department of Neurosurgery, Stanford University School of Medicine, MSLS Bldg., Room P306, 1201 Welch Rd., Stanford, CA 94305-5327, USA.
推荐引用方式(GB/T 7714):
Rong Xie,Peng Wang,Xunming Ji,et al.Ischemic post-conditioning facilitates brain recovery after stroke by promoting Akt/mTOR activity in nude rats[J].JOURNAL OF NEUROCHEMISTRY.2013,127(5):723-732.doi:10.1111/jnc.12342.
APA:
Rong Xie,Peng Wang,Xunming Ji&Heng Zhao.(2013).Ischemic post-conditioning facilitates brain recovery after stroke by promoting Akt/mTOR activity in nude rats.JOURNAL OF NEUROCHEMISTRY,127,(5)
MLA:
Rong Xie,et al."Ischemic post-conditioning facilitates brain recovery after stroke by promoting Akt/mTOR activity in nude rats".JOURNAL OF NEUROCHEMISTRY 127..5(2013):723-732