Neuroprotective potential of asprosin in traumatic brain ınjury: Histopathological and biochemical insights from an experimental rat model.

Surgical neurology international Pub Date : 2026-03-27 eCollection Date: 2026-01-01 DOI:10.25259/SNI_1049_2025
Ali Kaplan, Inan Gezgin, Demet Evleksiz, Gülru Esen, Ebru Annac, Adem Dogan
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Abstract

Background: Traumatic brain injury (TBI) remains a leading cause of morbidity and mortality, yet pharmacological neuroprotection is still an unmet need. Asprosin, a recently identified fasting-induced adipokine, has been implicated in oxidative stress modulation, apoptosis, and metabolic regulation. This study aimed to investigate the neuroprotective role of asprosin in an experimental rat model of TBI.

Methods: Thirty-two male Wistar rats were randomized into four groups: Control, Trauma, Trauma+Asprosin, and Asprosin. Moderate head trauma was induced using a validated closed-head injury model. Asprosin (10 µg/kg, intraperitoneal) was administered immediately and 12 h post-trauma. Brain tissues were examined histopathologically (cresyl violet staining) and biochemically for oxidative stress and apoptotic markers, including Glutathione, total oxidant status, superoxide dismutase, Catalase, Malondialdehyde, glutathione peroxidase, nitric oxide, total antioxidant status, asprosin, and caspase-3.

Results: Histopathological evaluation revealed pronounced neuronal degeneration, vacuolization, and darkly stained nuclei in the Trauma and Trauma+Asprosin groups, whereas the control and asprosin-only groups preserved normal cortical and hippocampal architecture. Biochemically, no significant differences were observed among groups for oxidative stress parameters; however, caspase-3 levels were significantly higher in the Asprosin group compared to controls (P = 0.02). These findings suggest that while asprosin modulates apoptosis-related pathways, its direct protective effect against trauma-induced neuronal damage remains inconclusive.

Conclusion: This study provides the first experimental evidence linking asprosin to TBI. Although asprosin demonstrated potential interactions with oxidative and apoptotic processes, its role as a neuroprotective agent requires further validation with larger cohorts, varied dosing regimens, and molecular analyses.

asprosin在创伤性脑中的神经保护潜力ınjury:来自实验大鼠模型的组织病理学和生化见解。
背景:创伤性脑损伤(TBI)仍然是发病率和死亡率的主要原因,但药理神经保护仍然是一个未满足的需求。Asprosin是最近发现的一种空腹诱导的脂肪因子,与氧化应激调节、细胞凋亡和代谢调节有关。本研究旨在探讨阿斯木蛋白酶在实验性脑外伤大鼠模型中的神经保护作用。方法:32只雄性Wistar大鼠随机分为4组:对照组、外伤组、外伤+阿斯普罗松组和阿斯普罗松组。采用经过验证的闭式颅脑损伤模型诱导中度颅脑损伤。立即和外伤后12小时给予阿斯匹辛(10µg/kg,腹腔注射)。对脑组织进行组织病理学(甲酚紫染色)和生化检查,检测氧化应激和凋亡标志物,包括谷胱甘肽、总氧化状态、超氧化物歧化酶、过氧化氢酶、丙二醛、谷胱甘肽过氧化物酶、一氧化氮、总抗氧化状态、asprosin和caspase-3。结果:在创伤组和创伤+阿斯普罗松组中,组织病理学检查显示明显的神经元变性、空泡化和细胞核黑色染色,而对照组和仅阿斯普罗松组保留了正常的皮层和海马结构。生物化学方面,各组氧化应激参数无显著差异;然而,Asprosin组的caspase-3水平明显高于对照组(P = 0.02)。这些发现表明,虽然阿霉素调节凋亡相关途径,但其对创伤性神经元损伤的直接保护作用仍不确定。结论:本研究首次提供了阿斯球蛋白与脑外伤相关的实验证据。尽管asprosin已证实与氧化和凋亡过程有潜在的相互作用,但其作为神经保护剂的作用还需要通过更大的队列、不同的给药方案和分子分析来进一步验证。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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