STEMedicine https://stemedicine.org/index.php/stem <p><strong>STEM</strong><strong>edicine (ISSN 2705-1188)</strong> is an Open Access, peer-reviewed journal published by <a href="http://www.innovationpublishing.org/" target="_blank" rel="noopener">Innovation Publishing House Pte. Ltd.</a> on a quarterly basis under the CC BY 4.0 license. We established <em>STEMedicine </em>with the goal to bring researchers and practitioners together on our platform, in order to share scientific discoveries and technological advances both in biology and medicine.</p> Innovation Publishing House Pte. Ltd. en-US STEMedicine 2705-1188 <p>Authors retain full copyright to their individual works, and publishing rights without restrictions.</p> <p>In accordance with the <a href="https://www.budapestopenaccessinitiative.org/">Budapest Open Access Initiative</a>, articles published in <em>STEMedicine</em> are freely available "on the public internet, permitting any users to read, download, copy, distribute, print, search, or link to the full texts of these articles, crawl them for indexing, pass them as data to software, or use them for any other lawful purpose, without financial, legal, or technical barriers other than those inseparable from gaining access to the internet itself. The only constraint on reproduction and distribution, and the only role for copyright in this domain, should be to give authors control over the integrity of their work and the right to be properly acknowledged and cited."</p> <p>Except where otherwise noted, all content on this website is licensed under a <a href="https://creativecommons.org/licenses/by/4.0" target="_blank" rel="noopener">Creative Commons Attribution 4.0 License</a>. This license allows for commercial and non-commercial redistribution as well as modifications of the work as long as attribution is given to the authors and <em>STEMedicine</em> as the original publication source, and a link to the article on the <em>STEMedicine</em> website is provided.</p> Protective effects of quercetin on traumatic brain injury-induced inflammation and oxidative stress in cortex through activating Nrf2/HO-1 pathway https://stemedicine.org/index.php/stem/article/view/189 <p><strong>Background:</strong>&nbsp;Traumatic brain injury (TBI) has been a serious public health issue. Clinically, there is an urgent need for agents to ameliorate the neuroinflammation and oxidative stress induced by TBI. Our previous research has demonstrated that quercetin could protect the neurological function. However, the detailed mechanism underlying this process remains poorly understood. This research was designed to investigate the mechanisms of quercetin to protect the cortical neurons.</p> <p><strong>Methods:</strong>&nbsp;A modified weight-drop device was used for the TBI model. 5, 20, or 50 mg/kg quercetin was injected intraperitoneally to rats at 0.5, 12, and 24 h post-TBI. Rats were sacrificed 3 days post-injury, and their cerebral cortex was obtained from the injured side. The rats were randomly assigned into three groups of equal number: TBI and quercetin group, TBI group, and Sham group. The brain water content was calculated to estimate the brain damage induced by TBI. Immunohistochemical and Western blot assays were utilized to investigate the neurobehavioral status. Enzyme-linked immunosorbent assay and reverse transcription polymerase chain reaction were performed to evaluate the inflammatory responses. The cortical oxidative stress was measured by estimating the activities of malondialdehyde, superoxide dismutase, catalase, and glutathione-Px. Western blot was utilized to evaluate the expression of nuclear factor erythroid 2-related factor 2 (Nrf-2) and heme oxygenase 1 (HO-1).</p> <p><strong>Results:</strong>&nbsp;Quercetin attenuated the brain edema and microgliosis in TBI rats. Quercetin treatment attenuated cortical inflammatory responses and oxidative stress induced by TBI insults. Quercetin treatment activated the cortical Nrf2/HO-1 pathway in TBI rats.</p> <p><strong>Conclusions:</strong>&nbsp;Quercetin ameliorated the TBI-induced neuroinflammation and oxidative stress in the cortex through activating the Nrf2/HO-1 pathway.</p> Jianqiang Song Guoliang Du Haiyun Wu Copyright (c) 2024 Jianqiang Song, Guoliang Du, Haiyun Wu https://creativecommons.org/licenses/by/4.0 2023-12-13 2023-12-13 5 1 e189 e189 10.37175/stemedicine.v5i1.189