Cottonseed Oil Alleviates Ischemic Stroke-Induced Oxidative Stress Injury Via Activating the Nrf2 Signaling Pathway
Cottonseed Oil Alleviates Ischemic Stroke-Induced Oxidative Stress Injury Via Activating the Nrf2 Signaling Pathway
复制标题
棉籽油通过激活 Nrf2 信号通路减轻缺血性中风引起的氧化应激损伤。
DOI：
10.1007/s12035-020-02256-y
复制
发表时间：
2021-01-14
影响因子：
5.1
通讯作者：
Mi, Weidong
中科院分区：
文献类型：
--
作者：
Liu, Min;Li, Hao;Mi, Weidong
氧化应激被认为是缺血性脑卒中损伤的主要原因之一，而核因子红细胞2相关因子2 （Nrf2）信号通路是最重要的内源性抗氧化应激损伤通路。棉籽油（CSO）主要用作脂溶性药物的溶剂，对外周组织损伤具有抗氧化作用。然而，CSO在缺血性卒中诱导的氧化应激损伤中的作用和机制以及Nrf2信号通路在很大程度上仍不清楚。在这项研究中，我们研究了CSO在调节大脑中动脉闭塞和再灌注（MCAO-R）或氧气和葡萄糖剥夺和再灌注（OGD-R）诱导的氧化应激损伤中的潜力。我们发现，每隔一天皮下注射一次1.3 mL/kg CSO治疗雄性大鼠，连续3周显著改善神经功能缺损；梗死体积减小；减轻神经元损伤；ROS和MDA含量降低；SOD、GSH、GSH- px活性升高；并显著增加Nrf2的表达。此外，10(-9)μ L/mL CSO作用于神经元细胞系（HT-22） 24 h可显著提高OGD-R损伤后的细胞活力，减少细胞凋亡；显著降低ROS和MDA水平；SOD、GSH、GSH- px活性升高；并诱导Nrf2核易位增加。基于我们的研究结果，我们得出结论，CSO治疗通过激活Nrf2信号通路减轻缺血性卒中损伤引起的氧化应激，突出了CSO作为缺血性卒中治疗的潜力。
Oxidative stress is believed to be one of the primary causes in ischemic stroke injury, and the nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway is the most important endogenous antioxidative stress damage pathway. Cottonseed oil (CSO), which is used mostly as a solvent for lipid-soluble drugs, has been shown to exert antioxidative effects against peripheral tissue injury. However, the effects and mechanisms of CSO on ischemic stroke-induced oxidative stress injury and the Nrf2 signaling pathway remain largely unknown. In this study, we investigated the potential of CSO in regulating oxidative stress injury induced by middle cerebral artery occlusion and reperfusion (MCAO-R), or oxygen and glucose deprivation and reperfusion (OGD-R). We found that 1.3 mL/kg CSO treatment of male rats with a subcutaneous injection once every other day for 3 weeks significantly improved neurological deficit; reduced infarction volume; alleviated neuronal injuries; reduced the content of ROS and MDA; increased the activity of SOD, GSH, and GSH-PX; and markedly increased the expression of Nrf2. Furthermore, treatment with 10(-9) mu L/mL CSO to a neuron cell line (HT-22) for 24 h significantly increased cell viability and decreased cell apoptosis after OGD-R injury; significantly reduced the levels of ROS and MDA; increased the activity of SOD, GSH, and GSH-PX; and induced an increase in Nrf2 nuclear translocation. Based on our findings, we conclude that CSO treatment alleviates ischemic stroke injury-induced oxidative stress via activating the Nrf2 signaling pathway, highlighting the potential that CSO has as a therapeutic for ischemic strokes.