PD98059 protects SH-SY5Y cells against oxidative stress in oxygen-glucose deprivation/reperfusion

被引:2
|
作者
Zhuge, Xiang-Zhen [1 ]
Hu, Wan-Xiang [1 ]
Liu, Yu-Mei [2 ]
Jiang, Chang-Yue [3 ,4 ]
Zhang, Xiao-Hua [1 ]
Chen, Meng-Hua [5 ]
Xie, Lu [1 ]
机构
[1] Guangxi Med Univ, Dept Physiol, Preclin Sci, 22 Shuangyong Rd, Nanning 350001, Guangxi, Peoples R China
[2] Shenzhen Bay Lab Neuropathy Inst China, Shenzhen 518107, Guangdong, Peoples R China
[3] HIV AIDS Clin Treatment Ctr Guangxi Nanning, Dept Pharm, Nanning 530000, Peoples R China
[4] Fourth Peoples Hosp Nanning, Nanning 530000, Peoples R China
[5] Guangxi Med Univ, Hosp 2, Inst Cardiovasc Dis, Nanning 530000, Guangxi, Peoples R China
基金
中国国家自然科学基金;
关键词
extracellular signal-regulated kinase; oxidative stress; mitochondria; apoptosis; ISCHEMIA-REPERFUSION INJURY; MITOCHONDRIAL FUSION; CEREBRAL-ISCHEMIA; SIGNALING PATHWAY; FISSION; INHIBITION; NEURONS; ERK1/2; RATS;
D O I
10.1515/tnsci-2022-0300
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Mitochondria play a key role in the cerebral ischemia-reperfusion injury. Although the extracellular signal-regulated kinase 1/2 inhibitor PD98059 (PD) is a selective and reversible flavonoid that can protect the mitochondria in a rat model of cardiac arrest/cardiopulmonary resuscitation, its role requires further confirmation. In this study, we investigated whether PD could maintain mitochondrial homeostasis and decrease reactive oxygen species (ROS) production in neuroblastoma (SH-SY5Y) cells exposed to oxygen-glucose deprivation/reperfusion (OGD/R). PD improved the mitochondrial morphology and function, reversed the increase in ROS production and cell apoptosis, and reduced total-superoxide dismutase and Mn-superoxide dismutase activities induced by OGD/R. PD decreases ROS production and improves mitochondrial morphology and function, protecting SH-SY5Y cells against OGD/R-induced injury.
引用
收藏
页数:12
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