Research Paper Volume 12, Issue 17 pp 17568—17581
HSPB8 overexpression prevents disruption of blood-brain barrier after intracerebral hemorrhage in rats through Akt/GSK3β/β-catenin signaling pathway
- 1 Department of Neurology, 2nd Xiangya Hospital, Central South University Changsha, Hunan Province, China
Received: December 28, 2019 Accepted: June 29, 2020 Published: September 4, 2020https://doi.org/10.18632/aging.103773
How to Cite
Copyright: © 2020 Hou 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.
Blood brain barrier (BBB) disruption is a crucial factor contributing to secondary brain injury after intracerebral hemorrhage (ICH). Heat shock protein B8 (HSPB8) has been recently reported to confer neuroprotection against against ischaemic stroke through maintaining BBB integrity. However, the role of HSPB8 in ICH is still elusive. In this study, we found that HSPB8 was upregulated by ICH and extensively expressed in neurovascular structure including endothelial cells and astrocytes. lentivirus intracerebroventricular (i.c.v) injection achieved a widespread and persistent HSPB8 overexpression in brain tissues. HSPB8 overexpression significantly ameliorated neurobehavioral deficits and brain edema at 24 and 72h following ICH. Moreover, HSPB8 overexpression remarkedly inhibited BBB disruption and significantly increase the level of p-Akt, p-GSKβ and intranuclear β-catenin 24h post-ICH. This effect was obviously reversed by Akt specific inhibitor, MK2206. Based on these findings, HSPB8 exerted its protective effect on BBB, at least partly, via Akt/ p-GSKβ/β-catenin pathways.