To study the effect of etanercept on retinopathy in diabetic rats and explore its mechanism.

Diabetic rat model was established by streptozotocin. The rats were randomly divided into control group (normal feeding), model group (diabetic rat model was established), experimental group (after modeling, etanercept 2 mg·kg^-1 was injected subcutaneously into the abdomen twice a week for 12 weeks), and combined group [based on the experimental group, 100 nmol·mL^-1 microRNA (miR)-30a inhibitor was injected into the tail vein]. The pathological morphology of retina was observed by hematoxylin-eosin staining. Enzyme-linked immunosorbent assay was used to detect the levels of serum inflammatory factors. The positive expression of glial fibrillary acidic protein (GFAP) in retinal of rats was detected by immunofluorescence staining. The relative expression level of miR-30a in retina was detected by reverse transcription real-time fluorescence quantitative polymerase chain reaction.

In the model group, pathological changes occurred in each layer of retina, while in the experimental group, the pathological changes were alleviated, retinal edema was alleviated, cell arrangement was more regular, and the structural boundaries of each layer were clear. In control group, model group and experimental group, the serum levels of interleukin-6 (IL-6) were (0.42±0.07), (1.21±0.16) and (0.69±0.11) μg·L^-1, respectively; the levels of IL-1β were (0.26±0.05), (1.82±0.29) and (0.74±0.16) μg·L^-1, respectively; the levels of tumour necrosis factor-α(TNF-α) were (0.49±0.08), (1.25±0.17) and (0.72±0.13) μg·L^-1, respectively; the relative expression levels of GFAP in retinal tissues were 1.00±0.17, 3.18±0.56 and 1.45±0.23, respectively; the relative expression levels of miR-30a in retinal tissues were 1.00±0.19, 0.61±0.10, and 0.89±0.15, respectively; there were statistical differences between the model group and the control group, and between the experimental group and the model group (all P<0.05).

Etanercept can reduce the level of inflammatory factors in diabetic rats, and has a protective effect on diabetic rats retinopathy, its mechanism may be related to the regulation of miR-30a to activate insulin receptor substrate 1/phosphatidylinositol 3 kinase/protein kinase B signaling pathway.