Format

Send to

Choose Destination
Brain Res. 2019 Jun 1;1712:7-15. doi: 10.1016/j.brainres.2019.01.043. Epub 2019 Feb 1.

Post-stroke gastrodin treatment ameliorates ischemic injury and increases neurogenesis and restores the Wnt/β-Catenin signaling in focal cerebral ischemia in mice.

Author information

1
Yunnan Key Laboratory of Stem Cell and Regenerative Medicine, Institute of Molecular and Clinical Medicine, Kunming Medical University, Kunming City 650500, Yunnan, China. Electronic address: qiucaiwei@kmmu.edu.cn.
2
School of Pharmaceutical Science, Kunming Medical University, Kunming City 650500, Yunnan, China.
3
Yunnan Key Laboratory of Stem Cell and Regenerative Medicine, Institute of Molecular and Clinical Medicine, Kunming Medical University, Kunming City 650500, Yunnan, China.
4
Experiment Enter for Medical Science Research, Kunming Medical University, Kunming City 650500, Yunnan, China.
5
City Administration of Dongying, Shangdong Agricultural High-tech Industrial Demonstration Zone, Dongying City 257000, Shangdong, China.
6
Department of Anatomy and Developmental Biology, Monash University, Clayton 3800, Australia. Electronic address: zhicheng.xiao@monash.edu.

Abstract

Cerebral ischemic stroke is one of the leading causes of death and disability worldwide, and the only available drug treatment is limited to a short window following the ischemic event. Gastrodin is the major bioactive constituent extracted from thetuberGastrodia elata, and is currently used to treat dizziness in the clinic. "Early" application of gastrodin (before modeling or immediately after ischemic injury) has shown antioxidative and neuroprotective effects in a transient focal brain ischemia model in rodents; however, it is not known whether the delayed administration of gastrodin after permanent focal cerebral ischemia ameliorates neural injury and increases neurogenesis. In this study, we performed a permanent middle cerebral artery occlusion (MCAO) model for the study of cerebral ischemic stroke in adult male mice to examine the effects of gastrodin. Gastrodin treatment that was started "late" (one day after the ischemic injury) significantly improved neural function, reduced infarct volume and apoptosis, and increased the number of DCX/BrdU double-positive cells in permanent MCAO mice. Moreover, gastrodin treatment markedly preserved the Wnt/β-Catenin signaling pathway, which could promote neurogenesis and provide neuroprotection brain injury. Our findings suggest that gastrodin treatment following ischemic injury can induce neuroprotection, promote neurogenesis and restored the Wnt /β-Catenin signaling pathway.

KEYWORDS:

Brain ischemia; Gastrodin; Neurogenesis; Neuroprotection; Wnt/β-Catenin signaling pathway

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center