101. Cottonseed Oil Alleviates Ischemic Stroke-Induced Oxidative Stress Injury Via Activating the Nrf2 Signaling Pathway
- Author
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Min Liu, Lixia Zhang, Hao Li, Yunming Xiao, Weidong Mi, Zhipeng Xu, Ruitong Chu, Yulong Ma, Yuxiang Song, Miao Sun, and Xiaoyan Wang
- Subjects
Male ,0301 basic medicine ,Cottonseed Oil ,NF-E2-Related Factor 2 ,Neuroscience (miscellaneous) ,Endogeny ,Pharmacology ,medicine.disease_cause ,Neuroprotection ,Rats, Sprague-Dawley ,Mice ,03 medical and health sciences ,Cellular and Molecular Neuroscience ,chemistry.chemical_compound ,0302 clinical medicine ,medicine ,Animals ,Viability assay ,Ischemic Stroke ,Cell Nucleus ,Neurons ,business.industry ,Glutathione ,Oxygen ,Oxidative Stress ,Protein Transport ,Glucose ,030104 developmental biology ,medicine.anatomical_structure ,Neurology ,chemistry ,Apoptosis ,Reperfusion Injury ,Neuron ,Signal transduction ,business ,030217 neurology & neurosurgery ,Oxidative stress ,Signal Transduction - Abstract
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 μL/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.
- Published
- 2021