Berberine protects against diabetic retinopathy by inhibiting cell apoptosis via deactivation of the NF‑κB signaling pathway.

A number of studies have reported that diabetic retinopathy (DR) is the major cause of blindness. Berberine (BBR) is a bioactive constituent that displays effects on blood glucose; however, the mechanism underlying the role of BBR during the development of DR is not completely understood. In the present study, a rat model of DR was successfully established. The eye tissues were removed and subsequently assessed by hematoxylin and eosin staining and the TUNEL assay. The catalase, malondialdehyde, reactive oxygen species, glutathione and superoxide dismutase contents of the eye tissues were measured. Müller cells were chosen for further in vitro experiments. Cell apoptosis was examined by Annexin V‑FITC apoptosis detection and Hoechst staining, and the mitochondrial membrane potential was assessed by JC‑1 mitochondrial membrane potential detection. BBR decreased ganglion cell layer, cell apoptosis, reduced diabetic‑induced oxidative stress and deactivated the NF‑κB signaling pathway in the rat model of DR. High glucose enhanced oxidative stress and induced mitochondria‑dependent cell apoptosis in Müller cells by activating the NF‑κB signaling pathway. BBR reversed the high glucose‑induced effects by decreasing the phosphorylation of IκB, inhibiting NF‑κB nuclear translocation and deactivating the NF‑κB signaling pathway. The results suggested that BBR protected against DR by inhibiting oxidative stress and cell apoptosis via deactivation of the NF‑κB signaling pathway; therefore, suggesting that BBR may serve as a promising therapeutic agent for DR.