Objective To observe the inhibition effect of curcumin on the proliferation of rabbit retinal pigment epithelial (RPE) cells and investigate its mechanism. Methods The 4th generation of RPE cells were selected and divided into curcumin group and blank control group. The concentration of curcumin included 10, 15, and 20 mu;g/ml. The MTT assay was used to evaluate the inhibition effect on the proliferation of RPE cells at the 24th, 48th, 72nd and 96th hour after cultured with curcumin (10, 15, and 20 mu;g/ml). The IC50 value of curcumin at different time points were calculated by Linear Regression. Flow cytometry was used to detect the effect on the cell cycle at the 72nd hour after cultured with curcumin (15 mu;g/ml); the expression and apoptosis of proliferating cell nuclear antigen (PCNA) were also determined at the 24th,48th, and 72nd hour after cultured with curcumin (15 mu;g/ml) respectively. The configuration of RPE cells were observed by transmission electron microscope. Results The IC50 value of curcumin at the 24th,48th, 72nd and 96th hour was 29.31, 17.50, 13.24, and 10.99 mu;g/ml respectively. Cell cycel analysis indicated that curcumin blocked cells in G0/G1 phase. At the 24th, 48th, and 72nd hour after cultured with curcumin (15 mu;g/ml), the expression of PCNA of RPE cells were 565.04plusmn;23.60, 473.61plusmn;36.88, and 396.15plusmn;32.45; the apoptosisrate were （12.83plusmn;0.13）%，（32.27plusmn;4.51）%，（56.81plusmn;8.67）%, respectively. The differeces of curcumin groups compared with the control group were significant (P＜0.05). Apoptosis of RPE cells was observed under transmission electron microscope. Conclusions Curcumin can inhibite the proliferation of RPE cells by inhibit the synthesization of PCNA and inducing the apoptosis of RPE cells. Curcumin may become a potential drug to prevent and treat PVR.
ObjectiveTo observe the longterm effect of suramin on the inhibition of proliferation of human retinal pigment epithelial (RPE) cells in vitro. MethodsRPE cells grown in 9 pieces of 96well plate (12 wells each plate) were divided into experimental and control group, with 6 wells in each group. The concentration of 0.1 ml RPE cells in each well is 5×104 cells/ml. After the change of the medium, RPE cells were treated with suramin (250 μg/ml) in experimental group while treated with nothing in the control group. The medium of the 2 groups were changed to the normal medium after 4 days. At the 1st, 2nd, and 4thday after the addition of suramin and at the 1st, 2nd, 3rd, 5th, 6th, 7th, 9th , 11th and 13th day after removing suramin, 1 plate was randomly selected to stop culturing, and the proliferation of RPE cells were detected by methyl thiazolyl tetrazolium (MTT) assay. ResultsUnder reversed microscope, RPE cells in control group were fused completely at the 7th day after inoculation. The extracellular space of RPE cells in experimental groups was larger than that in the control group, and remained unfused at the 13th day after inoculation. The inhibitory rate of proliferation of RPE cells at the first day after treated with suramin was 14.85% and increased to the highest 25.79% at the 4th day. The first day after the suramincontaining media was removed, the inhibitory rate decreased to 12.35%, and then raised gradually to over 20% at the 3rd to 5th day. Finally, the rate drop to 14.71%. ConclusionSuramin has the long-term effect on the inhibition of RPE cells induced by serum, especially the inhibitive effect after the remove of suramin, which indicates the specific double-peak inhibition during the whole process.(Chin J Ocul Fundus Dis, 2005,21:25-27)
Objective To observe the suppressive effect of co mbi nation of tissue plasminogen activator (t-PA), heparin and homoharringtonine on the formation of proliferative vitreoretinopathy (PVR) after vitreoretinal surgery. Methods Forty-three cases (44 eyes )of complicated retinal detachment who received vitreoretinal surgery were divided into 2 g roup s.Twenty cases(20 eyes)in group A were treated by intravitreal injection of abo ve mentioned drugs at the end of operation,while no intraocular injection of drugs given in 23cases(24 eyes)in group B.The mean follow-up period was 7.9 months. Result The rate of recurrent PVR in group A was 15.8%(3 of 19),and 45.5%(10 of 22) in group B (P＜0.05). The rate of recurrent retinal detachment was 5.5%(1 of 18) in group A,an d 33.3%(7 of 21) in group B，in group B(P＜0.05). Conclusion Combination use of the above mentioned drugs can effectively suppress the post operative recurrent PVR and lower the rate of subsequent recurrent retinal detac hment. (Chin J Ocul Fundus Dis, 2001,17:24-25)
Objective To investigate the therapeutic effects of subconjunctival verapamil on outcome in an experimental model of traumatic proliferative vitreoretinopathy. Methods An experimental model of traumatic proliferative vitreoretinopathy was induced in pigme nt rabbits,which then were selected randomly to receive either subconjunctival verapamil injection treatment or a placebo injection(control)daily for 3 weeks.Animals were examined by indirect ophthalmoscopy at weekly intervals for 5 weeks. Eyes were enucleated for light microscopy 5 weeks later. Results Fifty-six percent(18 of 32)of the rabbits receiving subconjunctival verapamil injection had developed tractional retinal detachment,whereas eighty-one percent(26 of 32)of control animals had developed tractional retinal detachment(chi;2=4.655,P=0.031).The results of clinical examination and light microscopy didn't show evidence of toxicity between the verapamil treated animals and control animals. Conclusion Subconjunctival verapamil decreased the incidence of tractional retinal detachment due to traumatic proliferative vetreoretinopathy in this rabbit model.Verapamil at the dose used in this model has no evident toxicity on rabbit eyes.Further studies are needed to determine the doseresponse and efficacy of the drug. (Chin J Ocul Fundus Dis,1999,15:69-71)