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Bilobalide protects astrocytes from oxygen and glucose deprivation-induced oxidative injury by upregulating manganese superoxide dismutase.

Authors
  • Xiang, Jun1, 2
  • Zhang, Jingsi1, 2
  • Cai, Xiaofang3
  • Yang, Feng1, 2
  • Zhu, Wen1, 2
  • Zhang, Wen1, 2
  • Cai, Min1, 2
  • Yu, Zhonghai1, 2
  • Li, Xiangting1, 2
  • Wu, Ting1, 2
  • Wang, Guohua1, 2
  • Cai, Dingfang1, 2
  • 1 Department of Integrative Medicine, Zhongshan Hospital Fudan University, Shanghai, China. , (China)
  • 2 Laboratory of Neurology, Institute of Integrative Medicine, Fudan University, Shanghai, China. , (China)
  • 3 Department of Stomatology, Zhongshan Hospital Fudan University, Shanghai, China. , (China)
Type
Published Article
Journal
Phytotherapy Research
Publisher
Wiley (John Wiley & Sons)
Publication Date
Sep 01, 2019
Volume
33
Issue
9
Pages
2329–2336
Identifiers
DOI: 10.1002/ptr.6414
PMID: 31243840
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Bilobalide (BB), a constituent of the Ginkgo biloba extract, is a neuroprotective agent with multiple mechanisms of action. To further explore the potential therapeutic effects of BB in stroke, we investigated its effects on primary astrocytes using the oxygen and glucose deprivation-reoxygenation (OGD-R) model. Cell viability was measured by lactate dehydrogenase release assay and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Cell death was measured by annexin 5 conjgated with fluorescein isothiocyanate (V-FITC) assay, and reactive oxygen species (ROS) production was measured by 2',7'-Dichlorodihydrofluorescein Diacetate (DCFH-DA) probe. Manganese superoxide dismutase (MnSOD) expression was measured by western blot and immunofluorescence. Mitochondrial membrane potential was monitored using JC-1 staining. Our results show that OGD-R downregulated MnSOD and impaired mitochondrial function, which further enhanced ROS production in primary astrocytes. As a result, cell viability was compromised, and cell death increased. BB treatment protected astrocytes from those injuries mainly by restoring MnSOD level as MnSOD inhibitor abolished the effects of BB. In conclusion, we demonstrated that OGD-R induced astrocytic injury, but BB increased the expression of MnSOD, the ROS scavenger, to reverse the exacerbated astrocytic injury. © 2019 John Wiley & Sons, Ltd.

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