科研之友
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摘要
A study was conducted using zebrafish as a model of hypoxic brain injury to investigate the potential neuroprotective effects of zinc (Zn2+) chelation. The accumulation of intracellular Zn2+ is a significant causal factor of the neuronal injury, and has been implicated in cell death followed by ischemic stroke. In this study, the zebrafish was placed in the hypoxia chamber with an extremely low level of dissolved oxygen (less than 0.8mg/L), which is similar to the conditions in a complete global ischemic stroke. Approximately 50% of zebrafish died after a short period (approximate to 11 min) of hypoxic treatment, suggesting that this is a responsive model system for use in evaluating treatments for hypoxic brain damage. The application of DEDTC reduced intracellular Zn2+ accumulation and produced a concentration-dependent effect by increasing the survival rate of zebrafish. Zn2+ chelation also enhanced zebrafish tolerance for hypoxia. When the brain damages were evaluated with TTC staining, the zebrafish that were treated with DEDTC in hypoxic treatment yielded the improvement of TTC staining that was similar to the healthy zebrafish brain. The results support that rising intracellular Zn2+ plays a critical role in the neuronal damages, and demonstrate the protective effects of Zn2+ chelation in hypoxic-ischemic brain injury in zebrafish.
- 出版日期2013-3
