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

Feb 5, 2019Brain research

Gastrodin treatment after stroke may reduce brain damage, boost new nerve growth, and restore key cell signaling in mice with localized brain ischemia

AI simplified

PubMed ↗DOI ↗

Abstract

Gastrodin treatment started one day after ischemic injury significantly improved neural function and reduced brain damage in a mouse model of stroke.

Delayed administration of gastrodin after permanent cerebral ischemia reduced infarct volume and apoptosis in mice.
Gastrodin increased the number of cells associated with neurogenesis, as indicated by a rise in DCX/BrdU double-positive cells.
The treatment preserved the Wnt/β-Catenin signaling pathway, which may be linked to neuroprotection and neurogenesis.
Findings indicate that gastrodin could have potential benefits even when administered after the onset of ischemic injury.

AI simplified

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.

Full Text

Full text is available at the source.

View full text (XML) ↗View full text ↗

Abstract

Full Text

Related papers

what lands in your inbox each week: