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Purpose: To explore the effects and molecular mechanism of action of curcumin on trabecular meshwork cells (TMCs). Methods: TMCs were isolated from pig eyes and NF-E2-related factor 2 (Nrf2) was knocked down by siRNA transfection. The effect of curcumin on intracellular reactive oxygen species (ROS) was measured by a ROS-specific dye. Annexin V-FITC/propidium iodide (PI) double labeling was applied to determine apoptosis. The expressions of apoptosis-associated proteins and Nrf2-Kelch-like ECHassociated protein 1 (Keap 1) pathway activation were assessed by western blotting, while target gene transcription was analyzed by quantitative real-time polymerase chain reaction (qRT-PCR). Results: Curcumin reduced the levels of intracellular ROS and apoptosis induced by H 2 O 2 , upregulated B-cell lymphoma-2 (Bcl-2), downregulated Bcl2-associated X (Bax), and activated caspase-3 and nine other proteins (p < 0.05). Curcumin reduced the expressions of Nrf2, HO-1, and NQO1, and increased Keap1 in H 2 O 2 -induced TMCs (p < 0.05). Moreover, Nrf2 knockdown partly reversed the effect of curcumin on ROS and apoptosis in TMCs induced by H 2 O 2 (p < 0.05). Conclusion: Curcumin inhibited oxidative stress and apoptosis by Nrf2-Keap1 activation in TMCs. Curcumin is therefore a potential therapeutic agent for the management of glaucoma. Keywords: Curcumin, Oxidative stress, Apoptosis, Glaucoma, Nrf2-Keap1

Curcumin protects trabecular meshwork cells against hydrogen peroxide-induced oxidative stress and apoptosis via Nrf2-keap1 pathway