PCO is an important cause of the gradual decline of visual acuity after cataract surgery. In terms of pathogenesis, because these residual cells are the cause of visual axis opacification, so remove of these cells during the surgery could reduce or eliminate the incidence of proliferation of LECs and the occurrence of PCO.
Zhang et al  study showed that IOLs were modified with ICG and then triggered by laser could obviously inhibit LECs proliferation and migration meanwhile other tissues in the eye were not affected in-vitro. In-vivo study found that ICG-IOL not only prevent PCO occurrence but also was safe for other tissues in the eye. Melendez et al  found that after LECs were cultured in 0.1 mg/mL ICG for 30 minutes, the cells were irradiated by 806-nm laser for 1 minute could significantly decrease cells activity. When the concentration of ICG reached 5 mg/mL, only less than 5% LECs survived. Therefore, we studied the effects of ICG on the apoptosis, proliferation, migration, invasion and transdifferentiation of HLECs and revealed the potential value of ICG in solving PCO.
Flow cytometry showed that ICG could promote HLECs apoptosis in a concentration-dependent manner. At present, the apoptosis signaling pathway induced by ICG is not clear. Therefore, this study assessed the relationship between ICG exposure and apoptosis in HLECs by research Bax, Bcl-2, caspase-3 and caspase-9, which are associate with controlling apoptosis events. The anti-apoptotic protein Bcl-2 inhibits apoptosis by decrease the level of cytochrome c release, while the pro-apoptotic protein Bax induces apoptosis by increase the level of cytochrome c release . The release of cytochrome c promotes the activation of caspase-9 , which then activates downstream caspases and causes cell apoptosis. The study revealed that ICG treatment leads to down-regulated of Bcl-2, while up-regulated of Bax, caspase-3 and caspase-9 expression, which may eventually lead to caspase-dependent cell death.
In this study, we evaluated the effect of ICG on HLECs proliferation, migration and invasion in vitro. The CCK-8, EdU assay and wound healing assay studies showed that HLECs were immediately affected after 3 minutes ICG treatment. Besides, the effect was concentration-dependent, in other words, higher concentrations of ICG leaded to more HLECs injure, and the inhibition effect was strongest when the ICG concentration was 1.5%. The occurrence of PCO requires the migration of equatorial LECs to the center of posterior capsule. The study results showed that the migration and invasion capabilities of HLECs were significantly decreased after ICG treatment. This can slow down the migration speed of HLECs to the posterior capsule. The EMT of LECs plays an important role in PCO formation. In the process of EMT, overexpression of α-SMA, N-cadherin, Fibronectin and Vimentin are considered key factors. Western blot showed that the expression of mesenchymal protein were decreased after ICG treatment. In conclusion, ICG may play a negative role in EMT by inhibiting mesenchymal protein expression.
In summary, ICG could not only promote the apoptosis of HLECs, but also inhibit the proliferation, migration, invasion and transdifferentiation of HLECs in a concentration-dependent manner. These preliminary results revealed that ICG might be a promising drug for the prevention of PCO in vivo application. However, further clinical studies are needed to assess the efficacy and tolerability of ICG when applied in the capsule bag.