Alteplase in preventing posterior capsule opacity by plasminogen activator inhibitor-1 and type i collagen expression inhibition in a posterior capsule opacity model with fibrin reaction in vitro: A experimental laboratory study

To investigate the effect of alteplase on plasminogen activator inhibitor -1 (PAI-1) and type I collagen expression in a posterior capsule opacity (PCO) model with fibrin reaction in vitro. Cultured human lens epithelial cells (HLEC) were isolated from the anterior lens capsule following a capsulotomy during cataract surgery. Cultured HLEC went into an in vitro wound scratch assay on fibrin coated dishes and were then divided into 4 groups consisting of a FBS 10% control group, and treatment groups of alteplase 25, 50 and 100 μg/ml. The effect of alteplase on plasminogen activator inhibitor (PAI-1) and type I collagen expression in PCO and its reaction with fibrin was investigated, determined by fluorescein intensity, labelled with fluorescein isothiocyanate (FITC) antibody of PAI-1 and type I collagen. The difference between expression levels among the groups was analyzed using a Kolmogorov-Smirnov test followed by a posthoc test showing a significance level of p<0.05. The lowest PAI-1 expression was obtained in the group treated with alteplase 100 ìg /ml (1.26 × 10⁶± 3.31 × 10⁵) compared to the control group (6.27 × 10⁶± 2.37 × 10⁵ , p= 0.00); a significant result was also obtained among treatment groups, and showed that inhibition behaves in a dose dependent way. All treatment groups significantly inhibited type I collagen as compared to control group (3.54 × 106 ± 8.28 × 105, p= 0.00), but the result is not significantly different among treatment groups. The inhibition effect of PAI-1 and type I collagen were influenced from the affects of several another pathways in type I collagen synthesis other than PAI-1. Alteplase showed an inhibition effect on PAI-1 and type I collagen with fibrin reaction in vitro in anterior lens capsule fibrosis, despite the inhibition effect on type I collagen not aligning with the inhibition of PAI-1.