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Abstract #106693 Published in IGR 23-3
Histone deacetylase 3 inhibitor attenuates diabetic retinopathy in mice
Jiang Y; Luo BJournal of neurophysiology 2023; 129: 177-183
Diabetic retinopathy is one of the most common microvascular complications of diabetes. Inhibition of histone deacetylase 3 (Hdac3) was proven to be a successful way to ameliorate central nervous system injury and vision problem in a glaucoma mouse model. However, its role in diabetic retinopathy remains largely unknown. Eight-week-old C57BL/6J mice were intraperitoneally injected with 50 mg of streptozotocin for 5 consecutive days to induce diabetes. After 1 wk, diabetic mice were selected and treated with Hdac3 inhibitor RGFP966 once every 3 days for 12 consecutive weeks. It was found that RGFP966 could decrease the mRNA and protein expression of Hdac3. It significantly increased diabetic retinopathy-reduced retinal thickness without affecting fasting blood glucose. It also decreased diabetic retinopathy-activated oxidative stress and cell apoptosis. Moreover, diabetic retinopathy mice displayed an increased expression of vascular endothelial growth factor and a decreased expression of glial fibrillary acidic protein, both of which were partially restored by RGFP966 treatment. Mechanically, RGFP966 decreased the expression of NADPH oxidase 2 (Nox2) whereas it increased the expression of superoxide dismutase 2 (Sod2) in diabetic retinopathy mice. In conclusion, RGFP966 significantly reduces oxidative stress, inflammation, and cell apoptosis in the retina of streptozotocin-induced diabetic mice, which may be associated with its modulation of Nox2 and Sod2 expression. The study demonstrated that RGFP966 significantly reduced oxidative stress, inflammation, and cell apoptosis in the retina of streptozotocin-induced diabetic mice, which may be associated with Nox2 and Sod2 expression.
Ophthalmology Department, Hefei Red Cross Eye Hospital, Hefei, Anhui, China.
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