Gentiopicroside attenuates diabetic retinopathy by inhibiting inflammation, oxidative stress, and NF-κB activation in rat model

Abstract

Diabetic retinopathy, an inflammatory condition, is one of the devastating complication associated with diabetes that can lead to irreversible blindness. Gentiopicroside (GP), a secoiridoid glycoside, exhibits anti-inflammatory and antioxidant activity. The investigation was carried out to explore whether GP could attenuate diabetic retinopathy in diabetic rats. Diabetes was induced by injecting streptozotocin (STZ) (65 mg/kg) intraperitoneally in 8-weeks-old male rats (200–240 g). The treatment group received GP (20, 40, 80 mg/kg) orally for a duration of 10 weeks in diabetic rats (n = 10), and the diabetic group animals received phosphate buffer solution (n = 20). Effect of GP on cell viability study was performed by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assay. Oxidative stress markers, inflammatory mediators, and angiogenic factors were quantified in the retinal tissues of diabetic animals. All data were analyzed by one-way analysis of variance (ANOVA) at P < 0.05. Cytoprotective effect of GP was observed in MTT assay. GP effectively downregulated inflammatory cytokine, nuclear factor κB (NF-κB), tumor necrosis factor-α (TNF-α), interleukin 1 beta (IL-1β), and intercellular adhesion molecules-1 (ICAM-1), and upregulated antioxidant markers glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT) in the retina of diabetic rats. GP equilibrated the disturbed angiogenic factors in the diabetic retinal tissues. Results clearly indicated defensive role of GP in the treatment of diabetic retinopathy by inhibition of NF-κB and oxidative stress.