International Journal of Neuroscience ( IF 2.2 ) Pub Date : 2020-11-04 , DOI: 10.1080/00207454.2020.1840374 Zhenghua Xiang 1 , Xiao-Hui Xu 2 , Gillian E Knight 3 , Geoffrey Burnstock 3, 4
Abstract
Introduction
The role of extra-hypothalamic thyrotropin-releasing hormone (TRH) has been investigated by pharmacological studies using TRH or its analogues and found to produce a wide array of effects in the central nervous system.
Methods
Immunofluorescence, In situ labeling of DNA (TUNEL), in situ hybridization chain reaction and quantitative real-time polymerase chain reaction were used in this study.
Results
We found that the granular cells of the dentate gyrus expressed transiently a significant amount of TRH-like immunoreactivity and TRH mRNA during the 6–24 h period following global cerebral ischemia/reperfusion injury. TUNEL showed that apoptosis of neurons in the CA1 region occurred from 48 h and almost disappeared at 7 days. TRH administration 30 min before or 24 h after the injury could partially inhibit neuronal loss, and improve the survival of neurons in the CA1 region.
Conclusion
These data suggest that endogenous TRH expressed transiently in the dentate gyrus of the hippocampus may play an important role in the survival of neurons during the early stage of ischemia/reperfusion injury and that delayed application of TRH still produced neuroprotection. This delayed application of TRH has a promising therapeutic significance for clinical situations.
中文翻译:
全脑缺血/再灌注损伤大鼠海马促甲状腺素释放激素肽和mRNA的瞬时表达
摘要
介绍
下丘脑外促甲状腺激素释放激素 (TRH) 的作用已通过使用 TRH 或其类似物的药理学研究进行了调查,并发现在中枢神经系统中产生广泛的影响。
方法
本研究使用免疫荧光、DNA 原位标记 (TUNEL)、原位杂交链式反应和定量实时聚合酶链式反应。
结果
我们发现,在全脑缺血/再灌注损伤后的 6-24 小时内,齿状回的颗粒细胞瞬时表达了大量的 TRH 样免疫反应性和 TRH mRNA。TUNEL显示CA1区神经元从48 h开始凋亡,7 d基本消失。损伤前30 min或损伤后24 h给药TRH可部分抑制神经元丢失,提高CA1区神经元存活率。
结论
这些数据表明,海马齿状回中短暂表达的内源性TRH可能对缺血/再灌注损伤早期神经元的存活起重要作用,延迟应用TRH仍能产生神经保护作用。TRH的这种延迟应用对临床情况具有有希望的治疗意义。