Sanguinarine induces apoptosis of human lens epithelial cells by increasing reactive oxygen species via the MAPK signaling pathway.

Posterior capsular opacification (PCO) remains a major complication of cataract surgery and is the most common reason for loss of vision. PCO is primarily associated with uncontrolled proliferation of residual human lens epithelial cells (HLEs). Sanguinarine is a type of benzophenanthridine alkaloid extracted from the herbaceous plant Sanguinaria canadensis, which is widely used for its anti‑microbial, anti‑inflammatory, anti‑oxidative and anti‑proliferative properties. However, studies examining the effect of sanguinarine on HLEs and the underlying mechanism are scarce. The present study aimed to investigate the effects of sanguinarine on HLEs. An MTT assay was used to determine the effect of sanguinarine on cell viability. Flow cytometry was used to evaluate cell apoptosis, and the mitochondrial membrane potential and reactive oxygen species (ROS) levels. A caspase 3/7 activity assay was also used to evaluate cell apoptosis, while western blotting was performed to determine protein levels. The results demonstrated that sanguinarine exerted an anti‑proliferative effect by inducing ROS, and caused cell apoptosis via mitochondrial and caspase‑dependent pathways. Treatment with sanguinarine led to the loss of mitochondrial membrane potential. Sanguinarine also significantly increased the phosphorylation levels of c‑Jun N‑terminal kinase and p38, which indicated the involvement of the mitogen‑activated protein kinase signaling pathway. These results suggested that sanguinarine may have a noteworthy pro‑apoptotic effect on HLEs, and may be used as a potential drug for PCO or even cataract prevention.