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Abstract #8351 Published in IGR 4-3
Neuroprotective effect of nipradilol on axotomized rat retinal ganglion cells
Nakazawa T; Tomita H; Yamaguchi K; Sato Y; Shimura M; Kuwahara S; Tamai MCurrent Eye Research 2002; 24: 114-122
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 15 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-labelled RGCs in flat-mounted retinas three 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.
T. Nakazawa, MD, Department of Ophthalmology, Tohoku University School of Medicine, Sendai, Japan. ntoru@fa2.so-net.ne.jp
Classification:
11.8 Neuroprotection (Part of: 11 Medical treatment)
