Research Paper Volume 14, Issue 6 pp 2574—2589
Progesterone attenuates neurological deficits and exerts a protective effect on damaged axons via the PI3K/AKT/mTOR-dependent pathway in a mouse model of intracerebral hemorrhage
- 1 Department of Neurosurgery, West China Medical School, West China Hospital, Sichuan University, Chengdu 610041, Sichuan Province, P.R. China
- 2 Department of Intensive Care Unit, The Affiliated Chengdu 363 Hospital of Southwest Medical University, Chengdu 610041, Sichuan Province, P.R. China
- 3 Department of Neurosurgery, Affiliated Hospital of North Sichuan Medical College, Nanchong 637002, Sichuan Province, P.R. China
- 4 Department of Neurosurgery, Chengdu Second People’s Hospital, Chengdu 610021, Sichuan Province, P.R. China
Received: March 31, 2021 Accepted: February 28, 2022 Published: March 19, 2022
https://doi.org/10.18632/aging.203954How to Cite
Copyright: © 2022 Liu 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
Intracerebral hemorrhage (ICH) is a devastating event with high disability and fatality rates. However, there is a lack of effective treatments for this condition. We aimed to investigate the neuroprotective and axonal regenerative effects of progesterone after ICH. For this purpose, an ICH model was established in adult mice by injecting type VII collagenase into the striatum; the mice were then treated with progesterone (8 mg/kg). Hematoma absorption, neurological scores, and brain water content were evaluated on days one, three, and seven after the ICH. The effect of progesterone on inflammation and axonal regeneration was examined on day three after the ICH using western blotting, immunohistochemistry, immunofluorescence, as well as hematoxylin-eosin, Nissl, and Luxol fast blue staining. In addition, we combined progesterone with the phosphoinositide 3-kinase/serine/threonine-specific protein kinase (PI3K/AKT) inhibitor, LY294002, to explore its potential neuroprotective mechanisms. Administration of progesterone attenuated the neurological deficits and expression of inflammatory cytokines and promoted axonal regeneration after ICH, this effect was blocked by LY294002. Collectively, these results suggest that progesterone could reduce axonal damage and produced partial neuroprotective effects after ICH through the PI3K/AKT/mTOR pathway, providing a new therapeutic target and basis for the treatment of ICH.