Kim Dongjoon, Hwang Hyoin, Shin Hyekyoung, Chung Yoonyoung, Jun Yong-Hyun
Department of Anesthesiology and Pain Medicine, Chosun University Hospital, Gwang-ju, Republic of Korea.
Institute of Well-Aging Medicare & Chosun University G-LAMP Project Group, Chosun University, Gwang-ju, Republic of Korea.
In Vivo. 2025 Sep-Oct;39(5):2609-2616. doi: 10.21873/invivo.14061.
BACKGROUND/AIM: The middle cerebral artery occlusion (MCAO) model is widely used to study stroke pathobiology. Dexmedetomidine (DEX) has demonstrated neuroprotective effects in ischemic brain models. Previous studies have shown that nuclear factor erythroid 2-related factor 2 (Nrf2) expression changes in the parietal cortex, which is supplied by the middle cerebral artery, after ischemic injury. While Nrf2 is known to regulate brain-derived neurotropic factor (BDNF) expression, its role in MCAO conditions has not been fully explored. This study aimed to investigate the effects of DEX on Nrf2 and BDNF expression in the parietal cortex following MCAO.
Mice were subjected to MCAO by inserting a silicone-coated suture into the common carotid artery. After 30 min, the suture was withdrawn to induce ischemia/reperfusion (IR) injury. Cortical brain tissues were harvested three days post-injury. Western blot analysis was performed to measure BDNF protein expression. The expression levels of the messenger ribonucleic acid (mRNA) Nrf2, pro-apoptotic protein (Bax), and anti-apoptotic protein (Bcl-2) were analyzed using quantitative real-time polymerase chain reaction.
The mRNA level of Nrf2 was significantly higher in the DEX group than in the MCAO group after three days of MCAO. BDNF protein expression (15 kDa) was also higher in the DEX group than in the MCAO group. Furthermore, Bax mRNA was lower, while Bcl-2 mRNA was higher in the DEX group than in the MCAO group.
DEX treatment up-regulated Nrf2 expression, which was associated with increased BDNF expression three days after MCAO.
背景/目的：大脑中动脉闭塞（MCAO）模型被广泛用于研究中风的病理生物学。右美托咪定（DEX）在缺血性脑模型中已显示出神经保护作用。先前的研究表明，在缺血性损伤后，由大脑中动脉供血的顶叶皮质中核因子红细胞2相关因子2（Nrf2）的表达会发生变化。虽然已知Nrf2可调节脑源性神经营养因子（BDNF）的表达，但其在MCAO情况下的作用尚未得到充分研究。本研究旨在探讨DEX对MCAO后顶叶皮质中Nrf2和BDNF表达的影响。
通过将硅胶涂层缝线插入颈总动脉对小鼠进行MCAO。30分钟后，拔出缝线以诱导缺血/再灌注（IR）损伤。在损伤后三天收集皮质脑组织。进行蛋白质免疫印迹分析以测量BDNF蛋白表达。使用定量实时聚合酶链反应分析信使核糖核酸（mRNA）Nrf2、促凋亡蛋白（Bax）和抗凋亡蛋白（Bcl-2）的表达水平。
MCAO三天后，DEX组中Nrf2的mRNA水平显著高于MCAO组。DEX组中BDNF蛋白表达（15 kDa）也高于MCAO组。此外，DEX组中Bax mRNA较低，而Bcl-2 mRNA较高。
DEX治疗上调了Nrf2的表达，这与MCAO三天后BDNF表达增加有关。
