Celastrol-based nanomedicine hydrogels eliminate posterior capsule opacification.

Aim: To formulate an injectable thermosensitive micelle-hydrogel hybrid system loaded with celastrol (celastrol-loaded micelle hydrogel: CMG) to prevent posterior capsule opacification (PCO). Materials & methods: Celastrol-loaded micelles were embedded in a thermosensitive hydrogel matrix to enable controlled on-demand celastrol delivery into the residual capsule. The efficacy and mechanisms of the system for eliminating PCO were evaluated in rabbits. Results: Celastrol-loaded micelles inhibited the migration and proliferation of lens epithelial cells induced by TGF-ß1. Celastrol prevents epithelial-mesenchymal transition in lens epithelial cells induced by TGF-ß1 through the TGF-ß1/Smad2/3/TEAD1 signaling pathway. In vivo efficiency evaluations showed that CMG demonstrated an excellent inhibitory effect on PCO in rabbits and had no obvious tissue toxicity. Conclusion: Injectable CMG may represent a promising ophthalmic platform for preventing PCO. This versatile injectable micelle-hydrogel hybrid represents a clinically relevant platform to achieve localized therapy and controlled release of drugs in other disease therapies.

Intraocular Lens with Mussel-Inspired Coating for Preventing Posterior Capsule Opacification via Photothermal Effect.

Phacoemulsification with implantation of intraocular lens (IOLs) has been widely applied as a standard treatment for cataract, which is the leading cause of vision impairment. However, it still remains a critical challenge to prevent posterior capsule opacification (PCO) in terms of postoperative visual quality. Herein, we report IOLs with mussel-inspired coatings for inhibiting lens epithelial cells and then preventing PCO through photothermal conversion effect. The mussel-inspired coatings are deposited on the nonoptical surface areas of IOLs, endowing the modified IOLs with efficient photothermal conversion property. The temperature can be facilely raised to 50-60 °C for the photothermal IOLs (PT-IOLs) by near-infrared (NIR) laser irradiation at a safe intensity of 0.3 W/cm2. These PT-IOLs display high capability of inhibiting lens epithelial cells (LECs) in vitro. Therefore, under routine NIR laser irradiation, New Zealand white rabbits implanted with the PT-IOLs demonstrate significantly lower evaluation of PCO (EPCO) scores than the control groups. The overall results indicate that our PT-IOLs provide a promising choice for the clinical prevention of PCO, thus opening a way to maintain the postoperative visual qualities for cataract patients.

Vitamin C decreases VEGF expression levels via hypoxia­inducible factor­1α dependent and independent pathways in lens epithelial cells.

Posterior capsular opacification (PCO) is the main complication following cataract surgery. The proliferation of the residual lens epithelial cells (LECs) serves an important role in PCO formation. The authors' previous study revealed that vitamin C inhibited the proliferation of human LECs by increasing the rapid degradation of hypoxia­inducible factor­1 (HIF­1α), and hence inhibited the expression of vascular endothelial growth factor (VEGF). The present study aimed to further investigate the mechanisms underlying the effects of vitamin C on the expression levels of VEGF. The present study demonstrated that the HIF­1 inhibitor BAY 87­2243 significantly inhibited the cell proliferation and the expression levels of VEGF in LECs through the use of colony formation, western blotting and ELISA assays. Moreover, it was revealed that vitamin C could further inhibit the cell proliferation and the expression levels of VEGF in LECs following the cotreatment with the HIF­1 inhibitor. The proline hydroxylation of HIF­1α by prolyl hydroxylases (PHDs) was previously discovered to be responsible for the rapid degradation of HIF­1α. Thus, the present study subsequently used three PHD inhibitors to investigate their effects on the expression levels of VEGF; it was found that the PHD2 specific inhibitor increased the expression levels of VEGF to the greatest extent. Moreover, the genetic knockdown of PHD2 by lentiviral transfection also significantly increased the expression levels of VEGF, whereas the PHD2 specific inhibitor did not alter the expression levels of VEGF in the PHD2 knockdown LECs. AKT kinase activity is an important mediator known to upregulate VEGF expression. Using an immunoprecipitation assay to isolate endogenous AKT, it was demonstrated that AKT was prolyl hydroxylated by PHD2, which inhibited its activity. It was also revealed that vitamin C enhanced the proline­hydroxylation and inhibited the activity of AKT. Furthermore, an AKT inhibitor increased the effects of vitamin C on the expression levels of VEGF. However, the AKT inhibitor did not affect the expression levels of glucose transporter 1, which is a HIF­1α target gene. In conclusion, the findings of the present study suggested that vitamin C may inhibit the expression levels of VEGF via HIF­1α­dependent and AKT­dependent pathways in LECs.

Aspirin inhibits TGFß2-induced epithelial to mesenchymal transition of lens epithelial cells: selective acetylation of K56 and K122 in histone H3.

Posterior capsule opacification (PCO) is a complication after cataract surgery that can disrupt vision. The epithelial to mesenchymal transition (EMT) of lens epithelial cells (LECs) in response to transforming growth factor ß2 (TGFß2) has been considered an obligatory mechanism for PCO. In this study, we tested the efficacy of aspirin in inhibiting the TGFß2-mediated EMT of human LECs, LECs in human lens capsular bags, and lensectomized mice. In human LECs, the levels of the EMT markers α-smooth muscle actin (α-SMA) and fibronectin were drastically reduced by treatment with 2 mM aspirin. Aspirin also halted the EMT response of TGFß2 when introduced after EMT initiation. In human capsular bags, treatment with 2 mM aspirin significantly suppressed posterior capsule wrinkling and the expression α-SMA in capsule-adherent LECs. The inhibition of TGFß2-mediated EMT in human LECs was not dependent on Smad phosphorylation or MAPK and AKT-mediated signaling. We found that aspirin significantly increased the acetylation of K56 and K122 in histone H3 of human LECs. Chromatin immunoprecipitation assays using acetyl-H3K56 or acetyl-H3K122 antibody revealed that aspirin blocked the TGFß2-induced acetylation of H3K56 and H3K122 at the promoter regions of ACTA2 and COL1A1. After lensectomy in mice, we observed an increase in the proliferation and α-SMA expression of the capsule-adherent LECs, which was ameliorated by aspirin administration through drinking water. Taken together, our results showed that aspirin inhibits TGFß2-mediated EMT of LECs, possibly from epigenetic down-regulation of EMT-related genes.

HSP90 as a novel therapeutic target for posterior capsule opacification.

Posterior capsule opacification (PCO) is a common complication of cataract surgery, resulting from a combination of proliferation, migration, epithelial-mesenchymal transition (EMT) of residual capsular epithelial cells and fibrosis of myofibroblasts. HSP90 is known to regulate the proteostasis of cells under pathophysiological conditions. The role of HSP90 in PCO formation, however, is not clear. To do this, the lens epithelial cell lines and an ex vivo cultured rat capsular bag model were used to study the role of HSP90 in PCO formation. The expression of protein and mRNA was measured by immunoblotting and quantitative RT-PCR, and cell apoptosis was measured by TUNEL(TdT-mediated dUTP nick-end labeling). The cell proliferation was measured by cell viability assays. The results showed that 17-AAG (Tanespimycin), an inhibitor of HSP90, suppresses the proliferation of immortalized lens epithelial cell lines HLE-B3, SRA01/04, and mLEC, with IC50 values of 0.27, 0.27, and 0.49 µM, respectively. In an ex vivo cultured rat capsular model, the capsular residual epithelial cells resisted the stress of the capsulorhexis surgery and took 3-6 days to completely overlay the capsular posterior wall. During this process, heat shock factor 1 and its downstream targets HSP90, HSP25, αB-crystallin, and HSP40 were upregulated. Treatment with 17-AAG inhibited the viability of capsular residual epithelial cells and induced the cells apoptosis, characterized by increases in ROS levels, apoptotic DNA injury, and the activation of caspases 9 and 3. HSP90 participated in regulating both EGF receptor (EGFR) and TGF receptor (TGFR) signaling pathways. HSP90 was found to interact with the EGFR, such that inhibition of HSP90 by 17-AAG destabilized the EGFR protein and suppressed p-ERK1/2 and p-AKT levels. 17-AAG also inhibited the TGF-ß-induced phosphorylation of SMAD2/3 and ERK1/2 and the decrease in E-cadherin and ZO-1 expression. Accordingly, these data suggest that the induction of HSP90 protects capsular residual epithelial cells against capsulorhexis-induced stress and participates in regulating the processes of proliferation, EMT and migration of rat capsular residual epithelial cells, at least partly, through the EGFR and TGFR signaling pathways. Treatment with 17-AAG suppresses PCO formation and is therefore a potential therapeutic candidate for PCO prevention.

ROCK inhibitor modified intraocular lens as an approach for inhibiting the proliferation and migration of lens epithelial cells and posterior capsule opacification.

Lens epithelial cells (LECs) in the capsule play a critical role in posterior capsule opacification (PCO) formation following cataract surgery. Cytoskeleton remodeling and the related ROCK pathway are quite important during cell migration and proliferation, but their role in LECs is still unclear. This study aimed to explore the mechanism of the ROCK pathway in the behavior of LECs and established a drug modified IOL for PCO prevention. We observed that the ROCK pathway inhibitor (Y27632) or cofilin knockdown reduced HLEC-B3 migration and proliferation. Furthermore, we revealed that cofilin could regulate the migration and proliferation of LECs through its phosphorylation. Interestingly, the capping protein CAPZA1 and ERM family also had an effect on the behavior of LECs. In addition, we established Y27632-PLGA modified IOLs, implanted them into rabbit eyes and found them to exhibit good safety and biocompatibility in vivo. Moreover, satisfying PCO prevention results were observed at 28 days post-operation. In summary, the ROCK pathway and the cytoskeleton remodeling protein regulate cell migration and proliferation, and the Y27632-PLGA modified IOL can prevent PCO formation.

The Intraocular Lens as a Drug Delivery Device: In Vitro Screening of Pharmacologic Substances for the Prophylaxis of Posterior Capsule Opacification.

Purpose: Numerous pharmacologic substances have been proposed for preventing posterior capsule opacification (PCO). The following trial was to compare those drugs to find more suitable options. IOL should then be modified by the pharmaceuticals as a drug-delivery device. Methods: A systematic literature search was performed to identify published substances. FHL-124 was used to determine cell proliferation and toxicity using a dye reduction test (XTT). Prescreened substances showing a reduction on cell growth without being toxic were soaked into an IOL. Those IOL were tested for their effect on PCO in an anterior-segment model and the human ex vivo capsular bag model. Toxicity on a corneal endothelial cell line (CEC-SV40) was determined. Release kinetics of methotrexate from the IOL was measured. Toxicity testing in both cell lines was done in serum-free conditions. All growth assays were exposed to 10% fetal calf serum (FCS)-supplemented medium. Results: The substances inhibited cell growth at the following EC50: caffeic acid phenethyl ester 1.6 ± 0.9 nM, disulfiram 359 ± 33 nM, methotrexate 98.0 ± 29.7 nM, rapamycin 70.2 ± 14.0 pM, and retinoic acid 1.1 ± 0.12 nM. All but disulfiram showed an effect in the anterior segment model when soaked into an IOL. Long-term inhibitory effects in the human capsular bag model were observed for caffeic acid phenethyl ester and methotrexate IOLs. Only methotrexate and disulfiram did not show any toxicity on endothelial cells. Methotrexate was released constantly from the hydrophilic IOL for 2 weeks. Conclusions: We could identify caffeic acid phenethyl ester and methotrexate in vitro as potential candidates for IOL modification for PCO prophylaxis.

Effect of an MG132-Sustained Drug Delivery Capsular Ring on the Inhibition of Posterior Capsule Opacification in a Rabbit Model.

PURPOSE: To design an MG132-sustained drug delivery capsular ring (SDDCR) and investigate its effect on the inhibition of posterior capsule opacification (PCO) in a rabbit model. METHODS: The SDDCRs were prepared by forming a slice of film made by the mixture of poly lactic-co-glycolic acid (PLGA) and MG132 on the surface of capsular tension rings (CTRs). The drug-loading capacity, entrapment efficiency, and in vitro release of the drug-containing film were detected. Eighteen New Zealand white rabbits were operated with phacoemulsification and MG132-SDDCRs/PLGA-CTRs/CTRs implantation in the single eye. The images of the anterior segments were acquired at certain days, and the epithelial-mesenchymal transition (EMT) markers were detected by western blot and immunofluorescence. RESULTS: The drug-loading capacity and entrapment efficiency of MG132-SDDCRs were 1.15% ± 0.04% and 66.16% ± 0.027%, respectively, and the drug released well within a month. The PCO degree of the MG132-SDDCR group was significantly lower than the other groups. The expression of alpha-smooth muscle actin, fibronectin, vimentin, and collagen-I was lower, and the expression of E-cadherin (E-cad) was higher in the MG132-SDDCR group than the other groups. CONCLUSIONS: MG132-SDDCRs could be established successfully. The PCO process was prevented, and the expression of EMT markers was inhibited by the implantation of MG132-SDDCRs, indicating that this could be a potential treatment against PCO.

The assessment of changes in macular thickness in diabetic and non-diabetic patients: the effect of topical ketorolac on macular thickness change after ND:YAG laser capsulotomy.

PURPOSE: The purpose of our study is to assess the changes in macular thickness (MT) in diabetic and non-diabetic patients and to research effects of topical ketorolac (Acular®, Allergan, Irvine, CA) on MT change after neodymium:yttrium aluminum garnet (Nd:YAG) laser capsulotomy. MATERIAL AND METHODS: This study involved 88 eyes of 88 patients diagnosed as posterior capsule opacification (PCO). Patients were divided into four groups according to presence of diabetes mellitus (DM) and drugs used after capsulotomy. Group 1: Patients with DM using only 0.1% Fluorometholon (FML®, Allergan, Irvine, CA) after capsulotomy (22 patients). Group 2: Patients with DM using 0.5% ketorolac (Acular®) and 0.1 Fluorometholon (FML®, Allergan, Irvine, CA) after capsulotomy (20 patients). Group 3: Patients without DM using only 0.1% Fluorometholon (FML®, Allergan, Irvine, CA) (22 patients). Group 4: Patients without DM using 0.5% ketorolac (Acular®) and 0.1% Fluorometholon (FML®, Allergan, Irvine, CA) (24 patients). A plus-shaped capsulotomy was performed using VISULAS® YAGIII (Carl Zeiss) laser microscope. MT measurement with Cirrus SD-OCT (Carl Zeiss Opthalmic System Inc., Model 400, Dublin, CA, Software 5) were done. Measurements were done before laser, and on the first day, first week, first month, third month and sixth month after laser capsulotomy. We compared the four groups for MT change during 6 months. RESULTS: Group 1 involving patients with DM using only 0.1% Fluorometholon (FML®, Allergan, Irvine, CA) after capsulotomy had increased MT at the first week, and the first, third, and sixth month after laser (p < 0.001). Group 3 involving patients without DM using only 0.1% Fluorometholon (FML®, Allergan, Irvine, CA) had increased MT at the first week, and at the first and third month, there was no statistically significant difference at the sixth month (p > 0.05). There was no statistically significant increase in MT during the follow-up period in group 2 involving patients with DM using 0.5% ketorolac (Acular®) and 0.1 Fluorometholon (FML®, Allergan, Irvine, CA) after capsulotomy and group 4 involving patients without DM using 0.5% ketorolac (Acular®) and 0.1% Fluorometholon (FML®, Allergan, Irvine, CA) (p > 0.05). CONCLUSION: An increase in MT can be observed after Nd:YAG laser capsulotomy, especially in diabetic patients. Adding topical ketorolac (Acular®, Allergan, Irvine, CA) to topical Fluorometholon (FML®, Allergan, Irvine, CA) therapy after YAG laser capsulotomy can prevent this increase.

Antibody-Drug Conjugate (ADC) Research in Ophthalmology--a Review.

Similar to cancer, many ocular proliferative disorders could be treated with a specific antibody conjugated to a toxin. Active targeting to inhibit epithelial and endothelial cell proliferation in the eye has been tested using antibody-drug conjugates (ADC) both pre-clinically and clinically. Achieving efficacious drug concentrations in the eye, in particular to treat back of the eye disorders is challenging, and the promise of targeted antibody mediated delivery holds great potential. In this review, we describe the research efforts in drug targeting using ADC for the treatment of choroidal neovascularization (CNV), posterior lens capsule opacification, and proliferative vitreoretinopathy. Among these disorders, CNV represents a more active research focus, with more target antigens tested, given the disease prevalence and wider target antigen selection based on current understanding of the pathophysiology of the disease. However, the only research advancing to testing in clinical stage is for posterior lens capsule opacification. Compared to oncology, ADC research and development in ophthalmology is much more limited, possibly due to availability of successful therapies that could be administered locally with limited concern of off-target drug toxicity.

Short-term effect of topical brinzolamide 1%-timolol 0.5% fixed combination on human central corneal thickness.

PURPOSE: To evaluate the short-term effect of fixed combination of brinzolamide 1% and timolol 0.5% (FCBT) application on human central corneal thickness (CCT). METHODS: This prospective clinical study included 97 patients having Nd:YAG laser posterior capsulotomy for posterior capsule opacification. Patients were randomized to receive apraclonidine hydrochloride 0.5% (APRA) (n=48) or FCBT (n=49) at 1 h before laser surgery. The baseline CCT was evaluated by ultrasonographic pachymetry from the central region ∼1 h before the laser procedure. CCT measurements were applied just before the laser application and then the first, second, and third hour, and the first, third, and seventh day after the Nd:YAG laser capsulotomy. RESULTS: There was no statistically significant difference between the baseline intraocular pressures, CCTs, and demographic and clinical data (age, sex, surgery laser interval, total laser energy) of the APRA and the FCBT groups. The mean CCT values of the APRA group at the first, second, and third hour, and the first, third, and seventh day were 553.8±28.0, 551.4±35.3, 556.8±28.7, 552.6±27.5, 548.2±26.2, and 546.2±25.5 µm, respectively. The mean CCT values of the FCBT group at the first, second, and third hour, and the first, third, and seventh day were 544.21±34.4, 549.4±27.6, 555.94±33.1, 550.8±33.4, 547.2±33.6, and 544.9±33.4 µm, respectively. No statistically significant difference was detected between the 2 groups. CONCLUSION: The difference in CCT increase between both groups was not statistically significant at any follow-up visits. FCBT application does not have a short-term effect on CCT.

[Intraocular lens as a drug delivery device]. / Intraokularlinse als Medikamententräger.

The development of an intraocular lens (IOL) as a drug delivery device has been the purpose of numerous preclinical studies and might become a future technology in cataract surgery. There are three techniques of pharmacological IOL modification: surface modification (coating), optic modification (soaking) or haptic modification with a slow-release-system. The therapeutic goals are endophthalmitis, postoperative inflammation and posterior capsule opacification.

Sulfadiazine modified PDMS as a model material with the potential for the mitigation of posterior capsule opacification (PCO).

Cataract surgery, while the most common surgical procedure performed, leads to posterior capsule opacification in approximately 30% of cases. Transforming growth factor beta 2 (TGF-ß2) and matrix metalloproteinases (MMPs) have been shown to play important roles in the cellular processes leading to posterior capsule opacification. Delivery of inhibitors to MMPs may have the potential to inhibit the initial cascade of events that lead to PCO. However, delivery of these molecules via tethering has proven difficult. In this work, sulfadiazine was tethered to polydimethylsiloxane (PDMS) via a polyethylene glycol (PEG) spacer as a potential MMPI mimic. Surface characterization using a variety of methods demonstrated successful modification with the antibiotic. The surfaces were examined with lens epithelial cells to determine their effect on these cellular processes, including cell transdifferentiation and production of extracellular matrix components. The presence of TGF-ß2 in the cell culture media was found to stimulate the production of ECM components such as collagen, fibronectin, and laminin, as well as alpha smooth muscle actin (α-SMA), and the migration marker Rho by HLE-B3 and FHL124 cells. In all cases, these effects were decreased but not completely eradicated by the presence of sulfadiazine on the PDMS surfaces. While the level of inhibition necessary for inhibition of PCO in vivo is unknown, these results suggest that IOL surface modification with sulfadiazine has the potential to reduce cellular changes associated with PCO. Furthermore, the results demonstrate for the first time that changes consistent with inhibition of fibrosis may be elicited by surfaces modified with sulfadiazine.

Modulation of matrix metalloproteinase activity by EDTA prevents posterior capsular opacification.

PURPOSE: To evaluate the effect of ethylenediaminetetraacetic acid (EDTA) on posterior capsular opacification (PCO) of rabbits and to assess its effect on intraocular tissues. METHODS: Modulation of matrix metalloproteinase (MMP) activity in the aqueous following cataract surgery in rabbits and its prevention by different doses of EDTA was determined by zymography. For evaluation of PCO, lensectomized rabbits were intracamerally injected with single dose of either 5 mg EDTA or normal saline. After one month, the degree of PCO was determined by slitlamp biomicroscopy, Miyake-Apple view, and histology of the lens capsule. The effect of EDTA on intra ocular pressure (IOP), corneal endothelial cells, and the retina was evaluated by tonometry, specular microscopy and scanning electron microscopy, and electroretinography. The concentration of EDTA in the aqueous was determined by high performance liquid chromatography (HPLC) at different time points. RESULTS: The MMP activity was significantly increased in the aqueous of the operated eyes, and EDTA reduced the degree of increase in a dose-dependent manner. EDTA treatment significantly reduced the degree of PCO (p<0.05). Histopathology of the lens capsule showed a reduction in the number of proliferating and migrating cells as well as MMP2 expression in the EDTA-treated eyes. EDTA treatment did not change the IOP; density, morphology and ultrastructure of the corneal endothelial cells; and electroretinography (ERG). EDTA was detectable in the aqueous humor up to 72 h following a single intracameral injection. CONCLUSIONS: EDTA reduces the degree of PCO by suppressing the MMP activity and it is not toxic to intra ocular structures at the concentration used.

Zebularine suppresses TGF-beta-induced lens epithelial cell-myofibroblast transdifferentiation by inhibiting MeCP2.

PURPOSE: Posterior capsular opacification (PCO) is a common long-term complication of modern cataract surgery. Remnant lens epithelial cells (LECs) undergo a myofibroblast transdifferentiation that is thought to be the initial step of PCO pathogenesis. The purpose of this study is to determine the effects of zebularine on transforming growth factor-ß (TGFß)-induced, LEC-myofibroblast transdifferentiation. METHODS: The expression levels of methyl CpG binding protein 2 (MeCP2) and α-smooth muscle actin (α-SMA) in human PCO membranes were evaluated by confocal microscopy. The role that MeCP2 played in TGFß2-induced α-SMA expression was analyzed by western blotting both before and after MeCP2 knockdown with MeCP2-specific siRNA. The effect of zebularine on MeCP2 expression was analyzed over time using a variety of dosages. The effect of zebularine on TGFß2-induced α-SMA expression was determined by western blot analysis. RESULTS: MeCP2 and α-SMA co-localized in human PCO membranes. When MeCP2 was depleted, TGFß2 could not induce α-SMA expression. Zebularine decreased MeCP2 expression in lens epithelial cells in a time- and dose-dependent pattern and reversed TGFß2-induced α-SMA expression. CONCLUSIONS: MeCP2 plays an important role in TGFß2-induced α-SMA expression in lens epithelial cells. Zebularine could reverse the TGFß2-induced α-SMA expression by inhibiting MeCP2 expression. Therefore, zebularine could potentially prevent PCO formation.

An experimental study on the effects of curcumin on posterior capsule opacification in young rabbit eyes.

BACKGROUND: Posterior capsule opacification (PCO) compromises vision development in infants after cataract surgery and lead to amblyopia. To observe the effects of curcumin on PCO in infant rabbits, curcumin was injected under the capaule and into the anterior chamber during phacoemulsification. METHODS: Seventy-five 1-month-old healthy New Zealand white rabbits were randomized into 3 groups, one eye of each rabbit was randomly selected to be operated. The operation involved continuous circular capsulorhexis, followed by hydrodissection with 0.6 ml each of balanced salt solution (BSS, group A), hydroxypropyl-ß-dodextrin (HP-ß-CD, 90 µg/ml, group B) or CUR-HP-ß-CD (123 µg/ml, group C), respectively. After phacoemulsification, 0.4 ml of each drug solution was injected into the anterior chamber via an incision. The extent of corneal edema and the inflammatory response within the anterior chamber were considered as measures PCO and observed postoperatively. All eyes were examined 1 and 2 months postoperative by slit lamp microscopy and photography after pupil dilation. On the third day postoperative, 6 rabbits from each group were executed. Paraffin-embedded sections were stained with hematoxylin-eosin (HE) or terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling assay (TUNEL, indicative of apoptosis). Stained sections were observed under light microscopy. Proliferation of lens epithelial cells (LECs) was observed microscopically on day 3, day 7, month 1 and month 2 after the operation with HE staining. RESULTS: The remission of cornea edema occurred earlier in group C than in groups A and B (P < 0.05); there were no significant differences between groups A and B. The remission of anterior chamber exudation in group C was earlier than those in groups A and B (P < 0.05). No significant difference in the times when PCO occurred, was observed among groups. Compared to groups A and B, the extent of PCO was less severe (P < 0.05). Three days after the operation, LECs aggregated at the orbit. Meanwhile, minor apoptosis was observed in all groups. One month after the operation transparent, cortex and proliferating LECs were observed near the orbit in groups A and B. Two months postoperative, heavy cortex proliferation was observed in all groups: epithelial cells migrated and aggregated at the posterior capsule and rearranged under the anterior capsule in the control group. Proliferation was also observed in group C, but to a less severe extent than in the other two groups. CONCLUSION: CUR-HP-ß-CD exerts an inhibitory effect on PCO.