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Customized Zebrafish Model of Hydrogen Peroxide-Induced Retina Damage

Oxidative damage plays a significant role in glaucoma onset and the imbalance between pro-oxidative and antioxidant capacities. The retinal injury model induced by oxidative stress is an excellent model to study oxidative damage related to glaucoma. In order to meet the research needs of our global customers, Ace Therapeutics has successfully established a zebrafish retinal oxidative damage model through vitreous H₂O₂ injection. This model can help our customers explore antioxidant protection therapies for glaucoma. Here, our researchers will spare no effort to pave the way for your glaucoma project to advance.

Zebrafish Models of Hydrogen Peroxide Induced Retina Damage

Glaucoma and Oxidative Damage

Glaucoma is an ocular neurodegenerative disease and one of the leading causes of blindness. The only current treatment option for glaucoma is lower intraocular pressure. However, accumulating evidence suggests that reactive oxygen species (ROS) play a key role in the pathogenesis of primary open-angle glaucoma (POAG), and intraocular pressure elevated (IOP) and local and systemic oxidative stress in optic nerve damage may be a risk factor for glaucoma development. ROS are involved in the pathogenesis of anterior and posterior ocular segment diseases in adults. Superoxide is produced directly from oxygen reduction, which is then converted to hydrogen peroxide. H₂O₂ can easily penetrate cell membranes and generate the most explosive oxygen form, the hydroxyl radical. An ideal model of oxidative stress in glaucoma can help researchers better understand glaucoma pathogenesis and develop new treatment options. Zebrafish larvae's retina is damaged by oxidative stress induced by IVT injection of hydrogen peroxide. This is a powerful tool for studying oxidative damage in glaucoma.

Fig. 1. 5 dpf larvae injected with 2 nl of various doses of H₂O₂ and fixed 8 hpi. (Giannaccini M, et al., 2018)

Service Overview

Glaucoma is a progressive optic neuropathy whose mechanism is related to oxidative stress on the retina and optic nerve head caused by elevated intraocular pressure. Increased ROS production, oxidative retinal damage, and an imbalance between pro-oxidative and anti-oxidative capacities are thought to be key factors in the onset of glaucoma. In view of this, Ace Therapeutics is committed to developing an oxidative damage model to help customers explore the link between oxidative stress and glaucoma and develop potential antioxidant protective therapies.

H₂O₂ is a commonly used substance to induce oxidative stress. In order to help our customers further understand the pathogenesis of oxidative damage in glaucoma, Ace Therapeutics successfully designs and develops an H₂O₂-induced oxidative stress model in zebrafish, which causes retinal damage accompanied by progressive neuronal death.

Explore Ace Therapeutics' Zebrafish Models of Hydrogen Peroxide-Induced Retina Damage

Ace Therapeutics induces a retinal injury model by injecting H₂O₂ into the vitreous of zebrafish larvae at 5 dpf. Given that glaucoma pathophysiology involves oxidative stress, this model could be useful in the design of neuroprotective or antioxidant therapies against RGC loss. To assess the situation in zebrafish, Ace Therapeutics monitors the endpoints of the zebrafish retinal injury model through the following pathways.

HE staining and histological evaluation.
Quantitative analysis of TUNEL-positive cells.
Qualitative and quantitative analysis of ganglion cells.
Active oxygen measurement.

Antioxidant protection therapy is another way to explore novel glaucoma treatments. Ace Therapeutics provides innovative zebrafish models of hydrogen peroxide-induced retina damage to advance your related projects. If you are interested in our services or need more detailed information, please feel free to contact us. Our experienced scientists are ready to help you!

References

Giannaccini M, Usai A, Chiellini F, et al. Neurotrophin-conjugated nanoparticles prevent retina damage induced by oxidative stress. Cell Mol Life Sci. 2018, 75(7):1255-1267.
Hsueh YJ, Chen YN, Tsao YT, et al. The Pathomechanism, Antioxidant Biomarkers, and Treatment of Oxidative Stress-Related Eye Diseases. Int J Mol Sci. 2022, 23(3):1255.

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