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Updated: Sep 29, 2026
Morphometric Analyses of Retinal Sections
Published on: February 19, 2012
Neuroprotective effect of nipradilol on axotomized rat retinal ganglion cells
Toru Nakazawa1, Hiroshi Tomita, Katsuhiro Yamaguchi
1Department of Ophthalmology, Tohoku University School of Medicine, Sendai, Japan. ntoru@fa2.so-net.ne.jp
Purpose:
To determine whether nipradilol, a new anti-glaucoma drug, can protect retinal ganglion cells (RGCs) from secondary cell death caused by transection of the optic nerve (ON).
Methods:
The ON was transected 0.7 mm from its exit from the eye in Sprague Dawley rats. Nipradilol (1 x 10(-8) - 10(-3) M), timolol, prazosin, or sodium nitroprusside (SNP) (1 x 10(-6) - 10(-4) M) was injected intravitreally fifteen-minutes before the ON transection. Control eyes received the same amount of phosphate buffered (PB). The RGCs were labeled retrogradely by placing gelfoam soaked in fluoro-gold (FG) on the stump of ON. RGCs density was determined by counting the FG-labeled RGCs in flat-mounted retinas 3 to 14 days post-transection. To determine whether the neuroprotective action of nipradilol was due to its NO-donor property, carboxy-PTIO, a NO-scavenger, or KT5832, a protein kinase G inhibitor, was injected with the nipradilol.
Results:
After ON transection, the number of surviving RGCs after intravitreal injection of 1 x 10(-4) M nipradilol was significantly higher than that following PB injection. This protective activity was dose-dependent. Neither timolol nor prazosin had a neuroprotective effect but SNP protected RGCs in a dose-dependent manner. Carboxy-PTIO and KT5832 decreased the neuroprotective effect of nipradilol.
Conclusions:
These results indicate that nipradilol has a possibility of neuroprotective effect on axotomized RGCs, and the effect depended mainly on its NO-donor property.
Insights
Nipradilol, an anti-glaucoma drug, demonstrated neuroprotective effects on retinal ganglion cells (RGCs) after optic nerve injury in rats. Its protective action is primarily linked to its nitric oxide-donating properties.
Area of Science:
- Ophthalmology
- Neuroscience
- Pharmacology
Background:
- Glaucoma is a leading cause of irreversible blindness.
- Retinal ganglion cells (RGCs) are crucial for vision and vulnerable to damage in glaucoma.
- Optic nerve transection serves as a model for studying RGC injury.
Purpose of the Study:
- To investigate the neuroprotective potential of nipradilol against secondary cell death in RGCs.
- To determine if nipradilol's neuroprotection is mediated by its nitric oxide (NO) donor properties.
Main Methods:
- Optic nerve transection was performed in Sprague Dawley rats.
- Nipradilol, timolol, prazosin, or sodium nitroprusside (SNP) were administered intravitreally.
- Retinal ganglion cell survival was assessed by counting fluoro-gold labeled RGCs post-transection.
- The role of NO was evaluated using a NO-scavenger (carboxy-PTIO) and a protein kinase G inhibitor (KT5832).
Main Results:
- Intravitreal nipradilol significantly increased RGC survival in a dose-dependent manner after optic nerve transection.
- SNP also exhibited dose-dependent RGC protection, unlike timolol or prazosin.
- Co-administration of carboxy-PTIO or KT5832 diminished nipradilol's neuroprotective effect.
Conclusions:
- Nipradilol demonstrates significant neuroprotective effects on axotomized RGCs.
- The neuroprotective mechanism of nipradilol is largely attributed to its nitric oxide-donating capability.
- Nipradilol shows promise as a therapeutic agent for protecting RGCs from injury.
