ArticleInternational journal of ophthalmology2013
Effects of aminoguanidine on retinal apoptosis in mice with oxygen-induced retinopathy.
Article in International journal of ophthalmology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed, 7 citations in OpenAlex.
- Aminoguanidine reduces diabetes-associated cardiac fibrosis.Experimental and therapeutic medicine · 2019Article
- Candesartan stimulates reparative angiogenesis in ischemic retinopathy model: role of hemeoxygenase-1 (HO-1).Angiogenesis · 2015Article
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6 authors at 1 institution in 1 country.
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Abstract
aimTo explore the protective effects of aminoguanidine (AG) on retinal apoptosis in mice with oxygen-induced retinopathy (OIR).
methodsA total of 80 C57BL/6J mice, aged 7 days, were randomly divided into four groups: normal, high oxygen, high oxygen saline and high oxygen treated with AG. In the normal group, mice were housed in normoxic conditions from postnatal day P7 to P17. Mice in the other 3 groups were placed under hyperoxic conditions (75±2%O2) in an oxygen-regulated chamber for 5 days and subsequently placed in normoxic conditions for 5 days. Mice in the AG group were treated once daily, from P12 to P17, with AG hemisulfate (100mg/kg body weight, intraperitoneally) dissolved in physiological saline. An equivalent amount of 0.9% physiological saline was administered, as above, to mice in the high oxygen saline group. Ten mice were randomly selected from each group on P14 and on P17, euthanized and the retinas examined. Apoptotic cells in the retina were detected using the terminal-deoxynucleoitidyl transferase mediated nick end labeling (TUNEL) method. The expression of nitric oxide synthase (iNOS) in the retina was detected by immunohistochemistry and changes in rod cells were observed using electron microscopy.
resultsTUNEL-positive cells and iNOS immunoreactive neurons were present in the inner nuclear and ganglion cell retinal layers of mice in the high oxygen group. The number of TUNEL-positive cells was significantly greater in the high oxygen group compared with the normal group (t=-20.81, P 14d <0.05; t=-15.05, P 17d <0.05). However, the number of TUNEL-positive cells in the AG treatment group was significantly lower (t=-13.21, P 14d<0.05; t=-6.61, P 17d <0.05) compared with the high oxygen group. The expression of iNOS was significantly higher in the high oxygen group compared with the normal group (t=-21.95, P 14d<0.05; t=-17.30, P 17d<0.05). However, the expression of iNOS in the AG treatment group was significantly lower (t=-12.17, P 14d<0.05; t=-10.30, P 17d<0.05) compared with the high oxygen group. The outer segments of the rods were disorganized and short in the high oxygen group. Rod morphology appeared to be slightly improved in the AG group.
conclusionAG may protect retinal neurons in OIR by inhibiting apoptosis. The mechanism may be related to iNOS.
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