Abstract
Ischemic conditioning inhibits oxidative stress and inflammatory response in diabetes. However, whether limb remote ischemic conditioning (LRIC) has beneficial effects on diabetic retinopathy (DR) remains unknown. This study aims to investigate the protective effects of LRIC in retinal ganglion cell in streptozotocin (STZ) induced Type 1 diabetic rats. A total of 48 healthy male Sprague-Dawley (200-220g) rats were randomly assigned to the normal group, normal+LRIC group, diabetes mellitus (DM) group and DM+LRIC group. Streptozotocin (STZ, 60 mg/kg) was intraperitoneally injected into the rats to establish the diabetic model. LRIC was conducted by tightening a tourniquet around the upper thigh and releasing for three cycles daily (10 mins x 3 cycles). Retinas were harvested after 12 weeks of LRIC treatment for histopathologic, Western blot and ELISA analysis. Plasma were collected at the same time for ELISA analysis. LRIC alleviated diabetic retinopathy symptoms as evidenced by the increased number of retinal ganglion cells (P<0.01) and decreased glial fibrillary acidic protein (GFAP) expression level (P<0.01) in the rat retina. LRIC in DM rats exhibited anti-inflammatory and antioxidative effects as confirmed by the down-regulation of pro-inflammatory cytokine: interleukin-6 (IL-6), and the up-regulation of antioxidants: superoxide dismutase (SOD), and glutathione (GSH)/oxidized glutathione (GSSG). Furthermore, LRIC significantly downregulated VEGF protein expression in the retina (P<0.01). These results suggest that the antioxidative and anti-inflammatory activities of LRIC may be important mechanisms involved in the protective effect of LRIC in STZ-induced diabetic rats.
Highlights
Diabetic retinopathy (DR), a leading cause of blindness, is one of the complications associated with diabetes [1]. increasing evidence support the idea that retinal neurons undergo degeneration, which may be part of vision impairment in the early stage of diabetes
We demonstrated that limb remote ischemic conditioning (LRIC) had a neuroprotective effect over diabetic retinopathy
This study suggests that LRIC could exert remarkable neuroprotective effects against diabetes-induced RGC degeneration in rats by attenuating the progression of diabetic retinopathy through anti-inflammatory and antioxidative mechanisms (Fig. 8)
Summary
Diabetic retinopathy (DR), a leading cause of blindness, is one of the complications associated with diabetes [1]. increasing evidence support the idea that retinal neurons undergo degeneration, which may be part of vision impairment in the early stage of diabetes. TNF- upregulated the expression of VEGF in the retina in early stages of diabetes, which was associated with increased vascular permeability and disruption of the blood-retinal barrier [8, 9]. Treatments that limit oxidative and inflammatory effects could be highly beneficial for DR patients by reducing or preventing retinal complications. Retinal ischemic conditioning induced by increasing intraocular pressure was reported to prevent and reduce retinal function impairment in both Type 1 and Type 2 diabetic animal models [12, 13]. Brandli et al reported that LRIC had a protective effect by significantly increasing the amplitude of a- and bwaves in a light-induced retinal damage animal model [15]. The aim of the present study was to examine whether LRIC has therapeutic effects in DR prevention by modulating oxidative stress and inflammation
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