Promotes HO-Induced Lens Epithelial Cells Oxidative Damage and Age-Related Cataract.

PURPOSE

To analyze the role of in lens epithelial cell oxidative damage and its underlying mechanism.

METHODS

Human lens epithelial cells (SRA01/04 cells) and rat transparent lens were cultured with HO to establish cell oxidative stress models and rat cataract models. Immunohistochemistry, quantitative real-time polymerase chain reaction (qRT-PCR), and Western blot assays were employed to detect levels within age-related cataracts(ARC) lens anterior capsule samples, rat cataract models, and cell oxidative stress models. In this study, qRT-PCR and Western blot assays were performed to derermine E-cadherin, N-cadherin, occludens1(ZO-1), α-SMA(α‑smooth muscle actin), Bcl-2, Bax, p-AKT, and AKT levels. In addition, Flow cytometry were performed to examine reactive oxygen species (ROS) and cell apoptosis. Cell viability, invasion, and migration were detected by CCK8, Transwell, and Wound healing.

RESULTS

Increased expression of was found in ARC lens anterior capsule samples, HO-induced rat cataract models, and Human lens epithelial cells (HLECs) oxidative stress models. HO significantly increased cell apoptosis and ROS generation, also accelerating cell migration, invasion, and epithelial-mesenchymal transition (EMT). In addition, HO treatment repressed AKT phosphorylation and cell viability. Knock-down of promoted cell viability and AKT phosphorylation levels, as well as repressed cell invasion, migration, apoptosis, ROS production and EMT.

CONCLUSION

promoted lens epithelial cells oxidative stress damage the AKT signalling pathways, providing a novel insight in ARC treatment.