PUBLICATION
In vivo brain ischemia-reperfusion model induced by hypoxia-reoxygenation using zebrafish larvae
- Authors
- Sawahata, M., Izumi, Y., Akaike, A., Kume, T.
- ID
- ZDB-PUB-210515-18
- Date
- 2021
- Source
- Brain research bulletin 173: 45-52 (Journal)
- Registered Authors
- Keywords
- blood flow, hypoxia, ischemia-reperfusion, stroke, zebrafish
- MeSH Terms
-
- Animals
- Animals, Genetically Modified
- Brain Ischemia/physiopathology*
- Cell Death/physiology*
- Cerebrovascular Circulation/physiology*
- Disease Models, Animal
- Neurons/physiology*
- Reperfusion Injury/physiopathology*
- Zebrafish
- PubMed
- 33989723 Full text @ Brain Res. Bull.
Citation
Sawahata, M., Izumi, Y., Akaike, A., Kume, T. (2021) In vivo brain ischemia-reperfusion model induced by hypoxia-reoxygenation using zebrafish larvae. Brain research bulletin. 173:45-52.
Abstract
Cerebral infarct is caused by cerebrovascular occlusion and results in brain damage. Although many rodent models of cerebral infarct exist, there is none based on zebrafish. In this study, we developed a novel ischemia-reperfusion model induced by hypoxic treatment using zebrafish. We first examined the changes in blood flow under hypoxic conditions. Hypoxic treatment interrupted the blood flow in 4 dpf (days post fertilization) zebrafish larvae. To quantify the trunk and cerebral blood flow, we selected the middle mesencephalic central artery (MMCtA) as a cerebral blood vessel and the dorsal aorta (DA) as a blood vessel of the trunk. Interestingly, the interruption of blood flow in MMCtA preceded that in DA. Considering these results, we hypothesized that reoxygenation immediately after hypoxia-induced cerebral ischemia leads to reperfusion. As a result, hypoxia-reoxygenation (H/R) treatment induced ischemia-reperfusion in cerebral vessels. Furthermore, brain cell death was increased 24 hours after H/R treatment. Transgenic zebrafish (HuC:kaede), with neuronal cells expressing the kaede fluorescent protein, was used to investigate the effect of H/R on neuronal cells. The H/R treatment reduced the fluorescence intensity of kaede. Besides, glial fibrillary acidic protein immunoreactivity in H/R-treated larvae was significantly increased. In conclusion, H/R-treated zebrafish larvae may provide a novel ischemia-reperfusion model.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping