@article{ref1,
title="Heat acclimation regulates the autophagy-lysosome function to protect against heat stroke-induced brain injury in mice",
journal="Cellular physiology and biochemistry",
year="2017",
author="Yi, Junfeng and He, Genlin and Yang, Ju and Luo, Zhen and Yang, Xuesen and Luo, Xue",
volume="41",
number="1",
pages="101-114",
abstract="BACKGROUND/AIMS: The mechanisms underlying the protective role of heat acclimation (HA) in heat stroke (HS)-induced brain injury are still unclear. The autophagy-lysosome pathway is known to pay an important role in protecting stressed or diseased cells from death. Nevertheless, whether autophagy and lysosomes are involved in HA-mediated neuroprotection following HS exposure remains unclear. <br><br>METHODS: The protective effects of HA were assessed by rectal temperature, hematoxylin-eosin staining, transmission electron microscopic analysis, terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling staining, and Fluoro Jade B staining, after mice were subjected to HS. The effects of HA on autophagy and lysosomes were assessed in the presence of the autophagy inhibitor 3-methyladenine (3MA). Autophagy and lysosome-associated proteins were analysed by Western blotting. <br><br>RESULTS: We found that HA protected against HS-induced death and brain injury. HS can robustly induce autophagy and impair lysosome function. HA pre-conditioning significantly modulated the autophagy level, and improved lysosome function in HS mice. Furthermore, 3MA completely abolished the neuroprotective effect of HA on HS. <br><br>CONCLUSION: HS may induce brain injury through lysosomal dysfunction and impaired autophagic flux. HA protected against HS-induced brain injury via a mechanism involving the autophagy-lysosome pathway.<br><br>© 2017 The Author(s)Published by S. Karger AG, Basel.<p /> <p>Language: en</p>",
language="en",
issn="1015-8987",
doi="10.1159/000455979",
url="http://dx.doi.org/10.1159/000455979"
}