Neuroprotective role of epigallocatechin-3-gallate in acute glaucoma via the nuclear factor-κB signalling pathway.

Abstract

Glaucoma is a disease involving impaired visual function accompanied by degeneration and necrosis of the optic nerve. Epigallocatechin-3-gallate (EGCG) exerts a neuroprotective effect against the degeneration of retinal ganglion cells. However, whether EGCG can relieve glaucoma and the possible mechanisms remain unclear. In order to determine the function of EGCG in glaucoma, an acute glaucoma rat model was established. Optic neuropathology was examined by haematoxylin-eosin staining and immunofluorescence staining for class III-β tubulin. The levels of inflammation-associated cytokines, such as interleukin (IL)-4, IL-6, TNF-α, IL-1β, IL-13 and IFN-γ were measured by flow cytometry. T cell proliferation was assessed by the carboxyfluorescein diacetate succinimidyl ester method. Finally, the functional role of EGCG in glaucoma was explored. The levels of the inflammation-associated proteins p-IκBα and p-p65 were measured by western blot analysis. The results showed that optic nerve injury occurred, and elevated levels of the inflammatory cytokines IL-4, IL-6, TNF-α, IL-1β, IL-13 and IFN-γ were observed in the rat model of acute glaucoma. In addition, an increased T lymphocyte proliferation rate and imbalance of Th1/Th2 cytokines were present in the models. Importantly, treatment with EGCG significantly alleviated optic nerve injury. At the molecular level, EGCG decreased the levels of inflammation-associated cytokines, decreased the proliferation rate of T lymphocyte cells, and repaired the imbalance of Th1/Th2 cytokines. Moreover, EGCG inhibited the increase in the phosphorylation of IκBα and p65 caused by modelling and thus suppressed the activation of the nuclear factor (NF)-κB signalling pathway. The findings of the present study indicate that EGCG could attenuate the symptoms of glaucoma and inhibit inflammatory responses by suppressing the NF-κB signalling pathway in a rat glaucoma model.