@article{ref1,
title="Tetrahydrocurcumin provides neuroprotection in rats after traumatic brain injury: autophagy and the PI3K/AKT pathways as a potential mechanism",
journal="Journal of surgical research",
year="2016",
author="Gao, Yongyue and Li, Jiang and Wu, Lingyun and Zhou, Chenhui and Wang, Qiang and Li, Xiang and Zhou, Mengliang and Wang, Handong",
volume="206",
number="1",
pages="67-76",
abstract="BACKGROUND: Tetrahydrocurcumin provides neuroprotection in multiple neurologic disorders by modulating oxidative stress, inflammatory responses, and autophagy. However, in traumatic brain injury (TBI), it is unclear whether a beneficial effect of tetrahydrocurcumin exists. In this study, we hypothesized that administration of tetrahydrocurcumin provides neuroprotection in a rat model of TBI. MATERIAL AND METHODS: Behavioral studies were performed by recording and analyzing beam-walking scores. The role of tetrahydrocurcumin on neurons death was assessed via Nissl staining. We then performed Western blot analyses, terminal deoxynucleotidyl transferase 2'-deoxyuridine-5'-triphosphate (dUTP) nick end labeling assays and immunofluorescence staining to evaluate autophagy and apoptosis. Phospho-protein kinase B (p-AKT) was also assessed via Western blotting. <br><br>RESULTS: Our data indicated that administration of tetrahydrocurcumin alleviated brain edema, attenuated TBI-induced neuron cell death, decreased the degree of apoptosis and improved neurobehavioral function, which were accompanied by enhanced autophagy and phospho-AKT after TBI. Moreover, the autophagy inhibitor 3-methyladenine and the PI3K kinase inhibitor LY294002 partially reversed the neuroprotection of tetrahydrocurcumin after TBI. <br><br>CONCLUSIONS: This study indicates that tetrahydrocurcumin protects neurons from TBI-induced apoptotic neuronal death, which may be through modulation autophagy and PI3K/AKT pathways. Thus, tetrahydrocurcumin may be an attractive therapeutic agent for TBI.<br><br>Copyright © 2016 Elsevier Inc. All rights reserved.<p /> <p>Language: en</p>",
language="en",
issn="0022-4804",
doi="10.1016/j.jss.2016.07.014",
url="http://dx.doi.org/10.1016/j.jss.2016.07.014"
}