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抑制NOX2有助于芦荟大黄素对创伤性脑损伤的治疗作用。

Inhibition of NOX2 contributes to the therapeutic effect of aloin on traumatic brain injury.

作者信息

Dong Haihai, Wang Haitao, Zhang Xuezhi

机构信息

Emergency Department, Anqiu People's Hospital, Weifang, China.

Department of Critical Care Medicine, Anqiu People's Hospital, Weifang, China.

出版信息

Folia Neuropathol. 2020;58(3):265-274. doi: 10.5114/fn.2020.100069.

DOI:10.5114/fn.2020.100069
PMID:33099296
Abstract

Traumatic brain injury (TBI) is a subset of brain injury induced by external mechanical forces to the head or neck. TBI has been reported to be one of the leading causes of disability, and it causes a huge financial burden around the world. Aloin is the major anthraquinone glycoside extracted from Aloe species, and has presented anti-tumour, anti-oxidative and anti-inflammatory activities. However, few studies have focused the effect of aloin in treatment of TBI. Nicotinamide adenine dinucleotide phosphate oxidase (NOX) is the only subset of enzymes which produces solely the reactive oxygen species (ROS). A recent study showed that activation of NOX might aggravate the primary TBI, and among these members, NOX2 is the key member in regulation of uncontrolled ROS expression, and thus plays a critical role in development of inflammatory diseases. Here, we noticed that inhibition of NOX2 combined with aloin treatment promoted the recovery of brain function in a mice model as well as the viability rate in a cell model. A further study found that the inflammation response process was also inhibited after treatment. Then, we found that these effects might be mediated by the PI3K/AKT/mTOR signalling pathway and NOX2 might be a therapeutic target for TBI.

摘要

创伤性脑损伤(TBI)是由头部或颈部受到外部机械力引起的脑损伤的一个子集。据报道,TBI是导致残疾的主要原因之一,并且在全球范围内造成了巨大的经济负担。芦荟素是从芦荟属植物中提取的主要蒽醌糖苷,具有抗肿瘤、抗氧化和抗炎活性。然而,很少有研究关注芦荟素在治疗TBI中的作用。烟酰胺腺嘌呤二核苷酸磷酸氧化酶(NOX)是唯一专门产生活性氧(ROS)的酶亚群。最近的一项研究表明,NOX的激活可能会加重原发性TBI,在这些成员中,NOX2是调节不受控制的ROS表达的关键成员,因此在炎症性疾病的发展中起关键作用。在这里,我们注意到,在小鼠模型中,抑制NOX2并联合芦荟素治疗可促进脑功能恢复以及细胞模型中的存活率。进一步的研究发现,治疗后炎症反应过程也受到抑制。然后,我们发现这些作用可能是由PI3K/AKT/mTOR信号通路介导的,并且NOX2可能是TBI的治疗靶点。

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