Fakharaldeen Zainab Ali, Al-Mudhafar Ahmed, Gany Sarmad Nory, Radhi Ali Nisoom, Hadi Najah Rayish
Department of Pharmacology and Therapeutics, Faculty of Medicine, University of Kufa, Najaf, Iraq.
Al-Hakeem Hospital, Al-Najaf Al-Ashraf, Iraq.
J Med Life. 2023 Oct;16(10):1534-1539. doi: 10.25122/jml-2023-0099.
This study aimed to investigate the potential neuroprotective effects of coenzyme Q10 in cerebral ischemia-reperfusion injury-induced neuronal damage and explore the underlying mechanisms. Twenty-eight adult male rats, weighing approximately 200-300 grams, were randomly divided into four groups: the sham group (neck dissection without ischemia), the control group (30 minutes of bilateral common carotid artery ligation followed by one hour of reperfusion), the vehicle group (oral carboxymethylcellulose solution for seven days prior to bilateral common carotid artery ligation and reperfusion), and the treatment group (seven days of coenzyme Q10 pretreatment followed by bilateral common carotid artery occlusion and reperfusion). Histopathological analysis and measurement of brain infarct size were performed, and cerebral levels of IL-6, IL-10, TNF-α, ICAM-1, NF-κB p65, and total antioxidant capacity were assessed. These cerebral tissue levels and cerebral infarct size were significantly elevated in the control and vehicle groups compared to the sham group. Conversely, the total antioxidant capacity was significantly reduced in these groups. Coenzyme Q10 treatment resulted in a significant increase in IL-10 and total antioxidant capacity levels, along with a significant decrease in IL-6, ICAM-1, TNF-α, and NF-κB p65 levels. Histopathological analysis revealed a significant reduction in ischemic damage in the coenzyme Q10-treated group. Coenzyme Q10 has neuroprotective properties in rats subjected to cerebral ischemia/reperfusion injury, possibly through its anti-inflammatory and anti-oxidative effects.
本研究旨在探讨辅酶Q10对脑缺血再灌注损伤所致神经元损伤的潜在神经保护作用，并探究其潜在机制。28只成年雄性大鼠，体重约200 - 300克，随机分为四组：假手术组（仅颈部解剖，无缺血）、对照组（双侧颈总动脉结扎30分钟，随后再灌注1小时）、溶剂组（在双侧颈总动脉结扎和再灌注前7天口服羧甲基纤维素溶液）和治疗组（辅酶Q10预处理7天，随后进行双侧颈总动脉闭塞和再灌注）。进行了组织病理学分析和脑梗死面积测量，并评估了大脑中白细胞介素-6（IL-6）、白细胞介素-10（IL-10）、肿瘤坏死因子-α（TNF-α）、细胞间黏附分子-1（ICAM-1）、核因子-κB p65（NF-κB p65）水平以及总抗氧化能力。与假手术组相比，对照组和溶剂组的这些脑组织水平和脑梗死面积显著升高。相反，这些组的总抗氧化能力显著降低。辅酶Q10治疗导致IL-10水平和总抗氧化能力显著升高，同时IL-6、ICAM-1、TNF-α和NF-κB p65水平显著降低。组织病理学分析显示，辅酶Q10治疗组的缺血损伤显著减轻。辅酶Q10对脑缺血/再灌注损伤的大鼠具有神经保护特性，可能是通过其抗炎和抗氧化作用实现的。
