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Effects of aminoguanidine on retinal apoptosis in mice with oxygen-induced retinopathy
An-Jie Du1, Bing Ren, Xiao-Wei Gao
1Ophthalmic Center, No. 474 Hospital of Chinese PLA, Urumqi 830013, Xinjiang Uygur Autonomous Region, China ; Department of Ophthalmology, Yuncheng Central Hospital, Yuncheng 044000, Shanxi Province, China.
Aim:
To explore the protective effects of aminoguanidine (AG) on retinal apoptosis in mice with oxygen-induced retinopathy (OIR).
Methods:
A 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.
Results:
TUNEL-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.
Conclusion:
AG may protect retinal neurons in OIR by inhibiting apoptosis. The mechanism may be related to iNOS.
Insights
Aminoguanidine (AG) reduces retinal apoptosis in oxygen-induced retinopathy (OIR) mice. This protective effect may involve the inhibition of inducible nitric oxide synthase (iNOS).
Area of Science:
- Ophthalmology
- Neuroscience
- Pharmacology
Background:
- Oxygen-induced retinopathy (OIR) is a significant cause of vision impairment.
- Retinal apoptosis and inflammation play crucial roles in the pathogenesis of OIR.
- Identifying therapeutic agents to mitigate OIR-related retinal damage is essential.
Purpose of the Study:
- To investigate the potential protective effects of aminoguanidine (AG) against retinal apoptosis in a mouse model of OIR.
- To explore the underlying mechanisms, particularly the role of inducible nitric oxide synthase (iNOS).
Main Methods:
- C57BL/6J mice were subjected to oxygen-induced retinopathy.
- Mice were treated with aminoguanidine (AG) or saline.
- Retinal apoptosis was assessed using the TUNEL assay.
- Inducible nitric oxide synthase (iNOS) expression was evaluated by immunohistochemistry.
- Rod cell morphology was examined using electron microscopy.
Main Results:
- Oxygen-induced retinopathy significantly increased retinal apoptosis and iNOS expression.
- Aminoguanidine (AG) treatment markedly reduced the number of apoptotic cells in the retina.
- AG administration also led to a significant decrease in iNOS expression.
- OIR caused disorganization of rod cell outer segments, with slight improvement observed after AG treatment.
Conclusions:
- Aminoguanidine (AG) demonstrates protective effects on retinal neurons in oxygen-induced retinopathy (OIR).
- The mechanism of protection appears to involve the inhibition of apoptosis.
- Inducible nitric oxide synthase (iNOS) may be a key mediator in AG's therapeutic action in OIR.
