• Ayşenur Sümer Coşkun, Mehmet Bülbül, Tuğçe Çeker, Ahmet Özak, Gamze Tanrıöver, İnanç Elif Gürer, Hazal Tuzcu Balaban, Ethem Göksu, and Mutay Aslan.
• Division of Anesthesia and Reanimation, Kepez State Hospital, 07320 Antalya, Turkey. Electronic address: anur.sumer@gmail.com.
• Neuroscience. 2024 Jul 23; 551: 307315307-315.

PurposeWe aimed to investigate early effects of exogenously administered adropin (AD) on neurological function, endothelial nitric oxide synthase (eNOS) expression, nitrite/nitrate levels, oxidative stress, and apoptosis in subarachnoid hemorrhage (SAH).MethodsFollowing intracerebroventricular AD administration (10 µg/5 µl at a rate of 1 µl/min) SAH model was carried out in Sprague-Dawley rats by injection of autologous blood into the prechiasmatic cistern. The effects of AD were assessed 24 h following SAH. The modified Garcia score was employed to evaluate functional insufficiencies. Adropin and caspase-3 proteins were measured by ELISA, while nitrite/nitrate levels, total antioxidant capacity (TAC) and reactive oxygen/nitrogen species (ROS/RNS) were assayed by standard kits. eNOS expression and apoptotic neurons were detected by immunohistochemical analysis.ResultsThe SAH group performed notably lower on the modified Garcia score compared to sham and SAH + AD groups. Adropin administration increased brain eNOS expression, nitrite/nitrate and AD levels compared to SHAM and SAH groups. SAH produced enhanced ROS/RNS generation and reduced antioxidant capacity in the brain. Adropin boosted brain TAC and diminished ROS/RNS production in SAH rats and no considerable change amongst SHAM and SAH + AD groups were detected. Apoptotic cells were notably increased in intensity and number after SAH and were reduced by AD administration.ConclusionsAdropin increases eNOS expression and reduces neurobehavioral deficits, oxidative stress, and apoptotic cell death in SAH model. Presented results indicate that AD provides protection in early brain injury associated with SAH.Copyright © 2024 IBRO. Published by Elsevier Inc. All rights reserved.

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