Abstract
Purpose :
Rhodopsin localization and rod photoreceptor (PR) morphology is altered across all models of Pro23His (P23H) retinopathy. Curcumin, a component of the Indian spice Turmeric, is neuroprotective to rod PRs in transgenic P23H rats and swine embryos and promotes normal trafficking of rhodopsin. We tested the hypothesis that curcumin therapy would prevent PR degeneration in P23H knock-in mice.
Methods :
Two litters of heterozygous P23H knock-in mice (n=14) and wild type (WT) littermates (n=4) were given curcumin (100 mg/Kg body weight) by oral gavage from postnatal (P) day 8 to P60. A third litter of untreated heterozygous mice (n=10) and WT (n=1) littermates were used as controls. At P60 retinal function was assessed using electroretinograms (ERGs), retinal ganglion cell (RGC) responses were recorded with the microelectrode array (MEA), and retinal morphology was evaluated using standard histology and immunohistochemistry.
Results :
Mean outer nuclear layer thickness was significantly reduced in untreated heterozygous P23H knock-in mice compared to curcumin-treated. Rhodopsin localization was similar in WT and curcumin-treated mice. Scotopic visual function was similar in both curcumin-treated and untreated mice and significantly reduced compared to WT. RGC responses were similar in both curcumin-treated and untreated mice.
Conclusions :
These data support a role for curcumin as a neuroprotective agent that delays morphological abnormalities that occur to rod PRs in a murine model of P23H retinopathy.
This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.