Purpose Diabetic retinopathy results from damage to small blood vessels and retinal neurons due to the overproduction of reactive oxygen species and overexpression of TRPM2 and TRPV1. Hence, inhibition of these events by ginger and selenium may reduce diabetes-induced ocular damage. Therefore, the aim of this study was to investigate the therapeutic effects of ginger, selenium, and their combinations on apoptosis, inflammation, insulin resistance, oxidative damage, and the expression of TRPM2 and TRPV1. Methods Seventy-two adult male Wistar rats were divided into nine groups as follows: control, diabetes, diabetes-ginger (100 mg/kg), diabetes-selenium (50, 100, and 150 µg/kg), and diabetes-ginger (100 mg/kg)–selenium (50, 100, and 150 µg/kg). Results Diabetes increased the expression of protein and genes of TRPM2 and TRPV1, and it induced oxidative damage by increasing malondialdehyde levels and decreasing superoxide dismutase, glutathione peroxidase, and catalase enzyme activities. Diabetes induced apoptosis by increasing BAX and caspase-3 gene expression and decreasing Bcl2 in eye tissue when compared to the control group. However, treatment with ginger (100 mg/kg), selenium (50, 100, and 150 µg/kg), and their combinations improved these situations in the diabetic groups compared to the diabetic group. Conclusions Diabetes induced retinopathy by inducing oxidative damage, inflammation, apoptosis, and upregulation of TRPM2 and TRPV1. However, treatments with selenium, ginger, and their combinations improved diabetic retinopathy by inhibiting oxidative damage, inflammation, and apoptosis and downregulating protein and gene expression of TRPM2 and TRPV1. The results of this study suggest that ginger and selenium can be a good treatment to inhibit the progression of diabetic retinopathy.
Huang et al. (Sun,) studied this question.