ORIGINAL RESEARCH article
Front. Neurol.
Sec. Neurotrauma
Volume 16 - 2025 | doi: 10.3389/fneur.2025.1551449
Neuroprotection Unveiled: Melatonin Mitigates Apoptotic Pathways in Traumatic Brain Injury
Provisionally accepted
- 1Koç University, Istanbul, Türkiye
- 2Mardin Artuklu University, Mardin, Mardin, Türkiye
- 3Dicle University, Diyarbakır, Diyarbakır, Türkiye
Select one of your emails
You have multiple emails registered with Frontiers:
Notify me on publication
Please enter your email address:
If you already have an account, please login
You don't have a Frontiers account ? You can register here
Objective: This study investigated the neuroprotective effects of melatonin in mice subjected to traumatic brain injury (TBI), focusing on caspase-dependent apoptotic signaling pathways.Materials and Methods: Twenty-one mice were divided into Control, TBI, and TBI + M groups. TBI was induced in TBI and TBI + M groups via free fall to the frontal lobes. Single dose of 10 mg/kg melatonin was intraperitoneally administered to the TBI + M group. Brain tissues were collected and subjected to histological evaluation and immunohistochemistry for apoptotic proteins.Results: Control group showed normal brain morphology, while Trauma group exhibited significant tissue loss and demyelination. TBI + M group showed reduced demyelination compared to Trauma group. Immunohistochemistry revealed increased Bax and decreased Bcl-2 expression in Trauma group, mitigated by melatonin treatment. Caspase-3 and caspase-9 expression was elevated in Trauma group, whereas TBI + M group showed levels comparable to Control.Melatonin at 10 mg/kg attenuated TBI-induced apoptosis and demyelination while promoting anti-apoptotic protein expression in the experimental model. These findings suggest a potential therapeutic role for melatonin in TBI management.
Keywords: Veri Sınıflandırma Tipi: Kurum İçi / Internal Traumatic brain injury, Melatonin, Apoptosis, neurodegeneration, Mice
Received: 08 Jan 2025; Accepted: 02 May 2025.
Copyright: © 2025 Gunara, Akgun, Seker, Ucar, Ates and Basar. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Mehmet Yigit Akgun, Koç University, Istanbul, Türkiye
Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.