Background/aims: The pathphysiological properties of N-Methyl -N -nitrosourea (MNU) induced photoreceptor degeneration are similar to the hereditary retinitis pigmentosa (RP). The present study sought to explore the beneficial effects of the peonidin, a common aglycone form of anthocyanin, on the MNU induced photoreceptor degeneration via topographic measurements.
Methods: The MNU administrated mouse received peonidin or vehicle injections, and then they were examined by electroretinography (ERG), multi electrode array (MEA), histological and immunohistochemistry studies.
Results: The protective effects of peonidin on the MNU administrated retinas were systematically verified and quantified by topographic measures. The peonidin treatment could protect the photoreceptor against the MNU toxicity both functionally and morphologicaly. The most sensitive zone to peonidin therapy was sorted out, indicating that different rescuing kinetics existed between the retinal hemispheres and retinal quadrants. Moreover, the hyperactive spontaneous firing response and the debilitated light induced response in MNU administrated retinas could be partially reversed by peonidin treatment. To our knowledge, this was the first study to explore the pharmacological effects of peonidin on the electrophysiological properties of inner visual signal pathways.
Conclusion: The peonidin could ameliorate the MNU induced photoreceptors degeneration and rectify the abnormities in the inner visual signal pathways. Future refinements of the knowledge cast insights into the discovery of a novel treatment for human RP.
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