Short communicationEffect of aminoguanidine on optic nerve involvement in experimental diabetic rats
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Acknowledgements
This study was supported by Grant-in-Aid 07671918 from the Ministry of Education, Science and Culture, Japan. The authors wish to thank Miss Na-omi Kurumaya, Mr. Hiroaki Naka and Mr. Hiroshi Kuriyama for their support during this experiment. The secretarial assistance of Miss Chinatsu Inotani is also acknowledged.
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2019, Experimental Eye ResearchCitation Excerpt :AGE accumulations in the optic nerve, around vessel and in cribriform plates, are also described in streptozotocin-induced diabetic rats, as well as in diabetic patients (Amano et al., 2001; Terai et al., 2012). AGE inhibitors partially reduced the level of glycation in the optic nerve in aged rhesus monkeys and in streptozotocin-induced diabetic rats (Ino-ue et al., 1998; Kiland et al., 2009). Degeneration of the trabecular meshwork leads to pathogenic elevated eye pressure in glaucoma, although the causes remain unknown.
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2009, Biochimica et Biophysica Acta - General SubjectsInvestigating structural and biochemical correlates of ganglion cell dysfunction in streptozotocin-induced diabetic rats
2009, Experimental Eye ResearchCitation Excerpt :Our findings confirm previous studies that have shown an increase in the percentage of connective tissue and blood vessels (Scott et al., 1986) and a reduction in myelin thickness (Ino-ue et al., 1998a, b), however they do not confirm reports of a reduction in axonal diameter (Ino-ue et al., 1998a, b) in the rat optic nerve. Studies by Ino-ue et al. (1998a, b) demonstrate that changes in the optic nerve were reversed using aminoguanidine (Ino-ue et al., 1998a), an inhibitor of advanced glycation end products (AGEs) and aldose reductase inhibitors (Ino-ue et al., 1998b), which can improve polyol metabolism, suggesting that AGEs/oxidative stress and polyol pathway metabolism may be involved in optic nerve changes. In the present study, alterations in optic nerve structure were not correlated with ganglion cell dysfunction, which argues that the locus of ganglion cell dysfunction after 12 weeks of STZ-induced diabetes might occur at the level of the retina.
Neuroprotective effect of aminoguanidine on iron-induced neurotoxicity
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