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Original Research

Systemic taurine treatment provides neuroprotection against retinal photoreceptor degeneration and visual function impairments

, , , , , , & show all
Pages 2689-2702 | Published online: 07 Aug 2019
 

Abstract

Objective

Retinitis pigmentosa causes progressive photoreceptor degeneration in the subjects while no clinical therapy exists. The present study sought to evaluate the potential protective effects of taurine on a pharmacologically induced RP animal model.

Methods

Photoreceptor degeneration in mice was induced by an intraperitoneal injection of N-methyl-N-nitrosourea (MNU). The MNU-administrated mouse received taurine treatment and then they were examined by electroretinography, spectral-domain optical coherence tomography, optokinetic test, and histological and immunohistochemistry assay.

Results

Prominent taurine deficiency was found in the retinas of MNU-administered mice. Intravenous taurine treatment increased significantly the retinal taurine level. Morphological studies showed that taurine could alleviate the retinal disorganizations in the MNU-induced mice. Taurine also ameliorated the visual impairments in the MNU-induced mice as evidenced by functional examinations. Immunostaining experiments demonstrated that both the M-cone and S-cone populations in the degenerative retinas are rescued by taurine. In particular, the M-cone photoreceptors in superior-temporal quadrant and the S-cone photoreceptors in inferior-nasal quadrant were preferentially rescued. Mechanism study showed that the photoreceptor apoptosis and oxidative stress in the degenerative retina were effectively alleviated by taurine treatment.

Conclusion

Taurine is protective against the MNU-induced photoreceptor degeneration. Systemic taurine administration may act as a promising therapeutic potion for retinopathies with chronic cycle.

Acknowledgments

This study is supported in part by the National Key Research and Development Plan of China [No. 2018YFA0107303] and National Natural Science Foundation of China [No. 81600767].

Disclosure

The authors report no conflicts of interest in this work.