RAB7L1 Participates in Secondary Brain Injury Induced by Experimental Intracerebral Hemorrhage in Rats

被引:0
作者
Xiaoxing Tan
Yuchong Wei
Jie Cao
Degang Wu
Niansheng Lai
Ruming Deng
Haiying Li
Haitao Shen
Ya Peng
Xiang Li
Gang Chen
机构
[1] The Third Affiliated Hospital of Soochow University,Department of Neurosurgery
[2] The First Affiliated Hospital of Soochow University,Department of Neurosurgery & Brain and Nerve Research Laboratory
[3] The First Affiliated Hospital of Wannan Medical College,Department of Neurosurgery
[4] The People’s Hospital of Bozhou,Department of Neurosurgery
来源
Journal of Molecular Neuroscience | 2021年 / 71卷
关键词
Intracerebral hemorrhage; Secondary brain injury; Rab7L1; Apoptosis;
D O I
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中图分类号
学科分类号
摘要
RAB7, a member of RAS oncogene family–like 1 (RAB7L1), is a GTPase belonging to the Rab family and acts as an upstream regulator to regulate the kinase activity of leucine-rich repeat kinase 2 (LRRK2). Although LRRK2 has been shown to aggravate secondary brain injury (SBI) after intracerebral hemorrhage (ICH), it is unknown whether RAB7L1 is also involved in this process. The purpose of the present study was to investigate the role of RAB7L1 in ICH-induced SBI in vivo. Autologous blood was injected into adult male Sprague-Dawley rats to induce an ICH model in vivo. The results showed that the protein levels of RAB7L1 increased after ICH. Overexpression of RAB7L1 induced neuronal apoptosis and damage, as demonstrated by TUNEL-positive and FJB-positive cells, and exacerbated ICH-induced learning and cognitive dysfunctions; in contrast, downregulation of RAB7L1 via RNA interference yielded comparatively opposite changes in these parameters. In summary, this study demonstrates that RAB7L1 promotes SBI after ICH and may represent a potential target for ICH therapy.
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页码:9 / 18
页数:9
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