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Abstract #21266 Published in IGR 10-2
Protective effect of aminoguanidine and betaxolol on retinal ischemia-reperfusion injury in rats
Ma Y-P; Zhu C-H; Hang HInternational Journal of Ophthalmology 2008; 8: 284-287
AIM: To observe the nitric oxide synthase (NOS) expression and measure the level of malondialdehyde (MDA) and to investigate the neuroprotective effect of NOS inhibitor aminoguanidine(AG) and betaxolol on rat retinal tissues in acute intraocular hypertension. METHODS: The ischemia-reperfusion injury models were established in 24 SD rats by increasing intraocular pressure through anterior chamber infusion. Three of 27 SD rats were randomly selected as blank controls. With intraocular hypertension persisting for 60 minutes, these 24 rats were subdivided into four groups: normal saline group, betaxolol treated group (2.5 g/L), AG treated group (100 mg/kg), and betaxolol + AG combined treatment group. Sagittal sections of optic nerves of right eyeballs were performed HE staining and retinal histology was observed at different time points after treatment. The NADPH-diaphorase reaction was employed to identify the NOS positive expression in the retina, and the contents of MDA were measured by TBA spectrophotometry. RESULTS: The-expressions of NOS were localized in retinas of all groups. In the retina, NOS positive cells mainly distributed in the retinal ganglion cell layer (GCL), inner plexiform layer (IPL) and inner nuclear layer (INL). The count of NOS positive cells in normal saline group was significantly more than that of the blank control group in retinal GCL (P < 0.01), while the number of NOS positive cells in AG, betaxolol treatment groups was less than that of normal saline group (P < 0.05). Moreover, the count of retinal NOS positive cells was positively correlated with the content of retinal MDA (r = 0.69, P < 0.01). CONCLUSION: By inhibiting the activity of iNOS, AG might protect the retina against acute ocular hypertension injury. In addition, betaxolol plays a role of neuroprotection by reducing intracellular overfreight of Ca2+, inhibiting the production of NO and enhancing the ability of anti-oxidation in retina. LA: Chinese
Dr. Y.-P. Ma, Department of Ophthalmolgy, Nanjing Medical University, Nanjing 210029 Jiangsu Province, China. Yanping_ma@163.com
Classification:
11.8 Neuroprotection (Part of: 11 Medical treatment)
5.1 Rodent (Part of: 5 Experimental glaucoma; animal models)
11.3.4 Betablocker (Part of: 11 Medical treatment > 11.3 Adrenergic drugs)