Xu Kai, Yang Zicheng, Shi Rongchen, Luo Chunxia, Zhang Zhiren
Institute of Immunology, Third Military Medical University of PLA, 30 Gaotanyan Main Street, Chongqing, 400038, People's Republic of China.
Department of Neurology, Southwest Hospital, Third Military Medical University, Chongqing, 400038, China.
Diagn Pathol. 2016 Aug 9;11(1):72. doi: 10.1186/s13000-016-0522-2.
Aryl Hydrocarbon Receptor (AhR) is a ligand-activated transcription factor with multiple functions operating in a variety of organs, including the brain. Recent studies have revealed that AhR played a functional role in traumatic injuries. This paper aims to study the expression of AhR during the early phase following a traumatic brain injury (TBI) in rat brains by immunohistochemistry.
Weight-drop induced TBI was performed in rats. The expression of AhR in brain of TBI rats were examined by immunohistochemistry.
Neuron expression of AhR in the rat brains of experiment group had been upregulated since day 3 in lesional hemisphere compared to that of the control group and mainly located in the cytoplasm, indicating an inactivated state. Interestingly, the accumulation of AhR(+) non-neuron cells became significant as early as 18 h after injury, which had kept increasing until 24 h post injury and then decreased slowly. For AhR(+) non-neuron cells, the AhR mainly located in cell nucleus, indicating a reactive status. Furthermore, double staining showed that most AhR(+) non-neuron cells co-localized with W3/13, a marker for T lymphocytes, but not with ED-1 (for activated microglia/macrophages) or GFAP (for activated astrocytes), suggesting that most AhR(+) non-neuron cells were T lymphocytes.
This is the first study concerning AhR expression in brains following TBI, and our data demonstrated that AhR was upregulated and activated in T lymphocytes following TBI. More research is needed to make a more conclusive conclusion.
芳烃受体(AhR)是一种配体激活的转录因子,在包括大脑在内的多种器官中发挥多种功能。最近的研究表明,AhR在创伤性损伤中发挥功能性作用。本文旨在通过免疫组织化学研究大鼠脑创伤性脑损伤(TBI)后早期阶段AhR的表达。
对大鼠进行重物坠落诱导的TBI。通过免疫组织化学检测TBI大鼠脑中AhR的表达。
与对照组相比,实验组大鼠脑损伤半球自第3天起AhR的神经元表达上调,且主要位于细胞质中,表明处于失活状态。有趣的是,AhR(+)非神经元细胞早在损伤后18小时就开始显著积聚,在损伤后24小时持续增加,然后缓慢下降。对于AhR(+)非神经元细胞,AhR主要位于细胞核中,表明处于反应状态。此外,双重染色显示,大多数AhR(+)非神经元细胞与T淋巴细胞标志物W3/13共定位,但不与ED-1(活化的小胶质细胞/巨噬细胞标志物)或GFAP(活化的星形胶质细胞标志物)共定位,表明大多数AhR(+)非神经元细胞是T淋巴细胞。
这是第一项关于TBI后脑内AhR表达的研究,我们的数据表明TBI后T淋巴细胞中AhR上调并被激活。需要更多的研究来得出更确凿的结论。