Abstract
Retinitis pigmentosa (RP) is an inherited photoreceptor-degenerative disease, and neuronal degeneration in RP is exacerbated by glial activation. Cassia seed (Jue-ming-zi) is a traditional herbal medicine commonly used to treat ocular diseases in Asia. In this report, we investigated the retina-protective effect of chrysophanol, an active component of Cassia seed, in an N-methyl-N-nitrosourea (MNU)-induced mouse model of RP. We determined that chrysophanol inhibited the functional and morphological features of MNU-induced retinal degeneration using scotopic electroretinography (ERG), optical coherence tomography (OCT), and immunohistochemistry analysis of R/G opsin and rhodopsin. Furthermore, TUNEL assays revealed that chrysophanol attenuated MNU-induced photoreceptor cell apoptosis and inhibited the expression of the apoptosis-associated proteins PARP, Bax, and caspase-3. In addition, chrysophanol ameliorated reactive gliosis, as demonstrated by a decrease in GFAP immunolabeling, and suppressed the activation of matrix metalloproteinase (MMP)-9-mediated gelatinolysis. In vitro studies indicated that chrysophanol inhibited lipopolysaccharide (LPS)-induced iNOS and COX-2 expression in the BV2 mouse microglia cell line and inhibited MMP-9 activation in primary microglia. Our results demonstrate that chrysophanol provided neuroprotective effects and inhibited glial activation, suggesting that chrysophanol might have therapeutic value for the treatment of human RP and other retinopathies.
Highlights
IntroductionFew studies have evaluated the protective effects of chrysophanol in the context of ocular diseases
Among the retinal degenerative diseases, Retinitis pigmentosa (RP) is hereditarily characterized by progressive rod and cone photoreceptor cell death
MNU induces the degeneration of the outer nuclear layer (ONL), a region abundant in photoreceptor cells, and this effect resembles the pathogenesis of end-stage human RP15
Summary
Few studies have evaluated the protective effects of chrysophanol in the context of ocular diseases. We investigated the retina-protective effects of chrysophanol in an N-methyl-N-nitrosourea (MNU)-induced mouse model of RP in vivo[15]. The MNU-induced mouse model of RP is a reliable and appropriate approach to investigate the neuroprotective effects and mechanisms mediated by bioactive compounds, such as chrysophanol, in RP. Chrysophanol prevented the functional and morphological features of MNU-induced photoreceptor apoptosis and retinal degeneration, and ameliorated glial activation. These findings suggest that the primary active component of Cassia seed, chrysophanol, has the potential to inhibit RP progression and prevent retinal injury. The mechanisms underlying this phenomenon, as well as the toxicity and long-term effects of chrysophanol, require further investigation
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
