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.