Fig. 8.

SRT1720 prevents diabetes-induced NeuN⁺ retinal decrease and improves visual and OKN response in db/db mice. (a, b) Chronic diabetes is associated with neuronal loss in the retina as demonstrated by reduced NeuN⁺ expression (green) in db/db mice when compared with non-diabetic db/m controls (a). Pharmacological SIRT1 activation using STR1720 in diabetic mice partly restores NeuN⁺ expression to control levels (a). Quantification shown in (b); n=4 from 3–5 sections at 100 µm interval for each eye with a minimum of four images per section; NeuN+ cells were quantified only in the GCL. (c) Analysis of the ERG showed diabetes-induced reduction of scotopic a- and b-waves; an increase and improvement in scotopic a- and b-wave was observed in diabetic mice treated with SRT1720 compared with diabetic mice on control chow. (d) An improvement in photopic b-wave was observed in diabetic mice treated with SRT1720 compared with diabetic mice on control chow; n=5–6 carried out from right and left eyes. (e) In diabetic mice, the OKN response is reduced compared with age-matched non-diabetic control mice. Diabetic mice treated with SRT1720 showed an improvement in visual acuity compared with diabetic mice on control chow; n=4–6 carried out from right and left eyes; *p<0.05, **p<0.01 ***p<0.001. Data are represented as mean ± SEM. Scale bar, 50 µm. Ctl, control (db/m); D, diabetic (db/db); GCL, ganglion cell layer; INL, inner nuclear layer; IPL, inner plexiform layer; ONL, outer nuclear layer; OPL, outer plexiform layer; PL, photoreceptor layer