Research Paper|Volume 13, Issue 4|pp 6134—6143

P2Y12 receptor-mediated microglia activation involved in delayed encephalopathy after acute carbon monoxide poisoning

Wenping Xiang¹, Zhigang Yang², Hui Xue¹, Jingbo Wang¹, Fanyan Niu¹, Jie Wang¹, Chao Chen¹, Yaming Wang¹, Jiangxia Pang¹, Baojun Wang¹

¹Department of Neurology, Baotou Central Hospital, Baotou 014040, Inner Mongolia, China
²Department of Urology, Baotou Central Hospital, Baotou 014040, Inner Mongolia, China

* Equal contribution

Received: October 28, 2020Accepted: December 10, 2020Published: February 20, 2021

https://doi.org/10.18632/aging.202607

Copyright: © 2021 Xiang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

To investigate the role of P2Y12 receptor-mediated microglia activation in delayed encephalopathy after acute carbon monoxide poisoning (DEACMP), we used static inhalation carbon monoxide to build DEACMP rat model. DEACMP rats were randomly assigned into DEACMP group and intervention group. A control goup was also set. The rats in intervention group received intraperitoneal injection of 100uM suramin (a P2Y12 receptor antagonist). In control group, the escape latency, level of microglia activation and ATP content were similar between different time points. In both DEACMP group and intervention group, the escape latency, level of microglia activation and ATP content were significanlty increased at 21th and 28th day. The hippocampal cells in DEACMP group and intervention group were severely and moderately, respectively, damaged at 21th and 28th day. Meanwhile, compared to control group, both DEACMP group and intervention group had significanlty longer escape latency, higher level of microglia activation and ATP content at 21th and 28th day. Compared to DEACMP group, the intervention group had significantly shorter escape latency and lower level of microglia activation at 21th and 28th day. These results suggested that the microglia activation regulated by ATP through P2Y12 receptor pathway might be closely related to the development of DEACMP.