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Philanthotoxin-343 attenuates retinal and optic nerve injury, and protects visual function in rats with N-methyl-D-aspartate-induced excitotoxicity

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dc.contributor.authorFazel M.F.en_US
dc.contributor.authorAbu I.F.en_US
dc.contributor.authorMohamad M.H.N.en_US
dc.contributor.authorAgarwal R.en_US
dc.contributor.authorIezhitsa I.en_US
dc.contributor.authorBakar N.S.en_US
dc.contributor.authorJuliana N.en_US
dc.contributor.authorMellor I.R.en_US
dc.contributor.authorFranzyk H.en_US
dc.date.accessioned2024-05-29T02:08:01Z
dc.date.available2024-05-29T02:08:01Z
dc.date.issued2020
dc.descriptionPLoS ONE15(7)en_US
dc.description.abstractRetinal ganglion cell (RGC) loss and optic neuropathy, both hallmarks of glaucoma, have been shown to involve N-methyl-D-aspartate receptor (NMDAR)-mediated excitotoxicity. This study investigated the neuroprotective effects of Philanthotoxin (PhTX)-343 in NMDAinduced retinal injury to alleviate ensuing visual impairments. Sprague-Dawley rats were divided into three; Group I was intravitreally injected with phosphate buffer saline as the control, Group II was injected with NMDA (160 nM) to induce retinal excitotoxic injury, while Group III was injected with PhTX-343 (160 nM) 24 h prior to excitotoxicity induction with NMDA. Rats were subjected to visual behaviour tests seven days post-treatment and subsequently euthanized. Rat retinas and optic nerves were subjected to H&E and toluidine blue staining, respectively. Histological assessments showed that NMDA exposure resulted in significant loss of retinal cell nuclei and thinning of ganglion cell layer (GCL). PhTX-343 pre-treatment prevented NMDA-induced changes where the RGC layer morphology is similar to the control. The numbers of nuclei in the NMDA group were markedly lower compared to the control (p<0.05). PhTX-343 group had significantly higher numbers of nuclei within 100 ?m length and 100 ?m2 area of GCL (2.9- and 1.7-fold, respectively) compared to NMDA group (p<0.05). PhTX-343 group also displayed lesser optic nerve fibres degeneration compared to NMDA group which showed vacuolation in all sections. In the visual behaviour test, the NMDA group recorded higher total distance travelled, and lower total immobile time and episodes compared to the control and PhTX-343 groups (p<0.05). Object recognition tests showed that the rats in PhTX-343 group could recognize objects better, whereas the same objects were identified as novel by NMDA rats despite multiple exposures (p<0.05). Visual performances in the PhTX-343 group were all comparable with the control (p>0.05). These findings suggested that PhTX-343 inhibit retinal cell loss, optic nerve damage, and visual impairments in NMDA-induced rats. Copyright � 2020 Fazel et al.en_US
dc.identifier.citationFazel MF, Abu IF, Mohamad MHN, Agarwal R, Iezhitsa I, Bakar NS, et al. (2020) Philanthotoxin-343 attenuates retinal and optic nerve injury, and protects visual function in rats with N-methyl-D-aspartate-induced excitotoxicity. PLoS ONE15(7): e0236450. https://doi.org/ 10.1371/journal.pone.0236450en_US
dc.identifier.doihttps://doi.org/10.1371/journal.pone.0236450
dc.identifier.isiWOS:000579931700045
dc.identifier.issn19326203
dc.identifier.issue7-Jul
dc.identifier.scopus2-s2.0-85088682793
dc.identifier.urihttps://www.scopus.com/inward/record.uri?eid=2-s2.0-85088682793&doi=10.1371%2fjournal.pone.0236450&partnerID=40&md5=008cf3153e6e2ad01d8581b162367620
dc.identifier.urihttps://journals.plos.org/plosone/article?id=10.1371/journal.pone.0236450
dc.identifier.urihttps://oarep.usim.edu.my/handle/123456789/10416
dc.identifier.volume15
dc.languageEnglish
dc.language.isoen_USen_US
dc.publisherPublic Library of Scienceen_US
dc.relation.ispartofPLoS ONEen_US
dc.sourceScopus
dc.titlePhilanthotoxin-343 attenuates retinal and optic nerve injury, and protects visual function in rats with N-methyl-D-aspartate-induced excitotoxicityen_US
dc.typeArticleen_US
dspace.entity.typePublication

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Philanthotoxin-343 attenuates retinal and optic nerve injury, and protects visual function in rats with N-methyl-D-aspartate-induced excitotoxicity
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