Neuroprotective effects of etanercept on diabetic retinopathy via regulation of the TNF-α/NF-κB signaling pathway

Purpose: To study the influence of etanercept on diabetic retinopathy in rats via tumor necrosis factor alpha (TNF-alpha)/nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappa B) signaling pathway. Methods: Thirty-six Sprague-Dawley (SD) rats were randomly divided into normal, model and etanercept groups. The expression of Caspase-3 was determined by immunohistochemistry, while the relative protein and mRNA expression levels of TNF-alpha and NF-kappa B were determined by Western blotting and quantitative polymerase chain reaction, respectively. Besides, the contents of TNF-alpha and interleukin-1 beta (IL-1 beta) were evaluated using enzyme-linked immunosorbent assay (ELISA), while cell apoptosis was assessed by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL). Results: Immunohistochemical studies showed that the mean optical density of tissues positive for caspase-3 in both the model and etanercept groups were significantly higher than in the normal group (p < 0.05), while the mean optical density in the etanercept group was significantly lower than that in the model group (p < 0.05). The protein expression levels of TNF-alpha and NF-kappa B in the etanercept group were significantly lower than those in the model group (p < 0.05). Furthermore, mRNA expressions of TNF-alpha and NF-kappa B declined in the etanercept group (p < 0.05); in addition, TNF-alpha, and IL-1 beta levels in the etanercept group were lower than in the model group (p < 0.05). Cell apoptosis in the etanercept group was also lower than in the model group. Conclusion: Etanercept suppresses TNF-alpha/NF-kappa B signaling pathway thereby repressing inflammation and cell apoptosis in diabetic retinopathy rats. Therefore, etenercept's neuroprotective effect may potentially be useful in developing a suitable therapy for diabetic neuropathy.

Automated summary

Etanercept suppresses inflammation and cell apoptosis in diabetic retinopathy rats by inhibiting the TNF-α/NF-κB signaling pathway.