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Objective: proliferative vitreoretinopathy (proliferative vitreo-retinopathy, PVR) is caused by a serious visual impairment or even blindness one eye. Retinal detachment, ocular trauma, diabetic retinopathy and other diseases are the main cause PVR. PVR is due to retinal pigment epithelial cells (retina pigment epithelial cells, RPE cells) and glial cells hyperplasia, in the vitreous and retina behind the proliferation of film formed on the surface fibers, fiber membrane contraction can cause extensive traction retinal detachment (traction retina detachment, TRD). If TRD is due to penetrating eye injuries after eye caused by overgrowth of fibrous tissue, it is called traumatic PVR, which is based on cell migration into the vitreous and retinal surface hyperplasia as the basic pathological features. Currently, although surgery can effectively remove PVR hyperplasia film, but it also destroys the blood - retinal barrier, the blood - aqueous barrier, the results inflammation weight, high recurrence rate. Search for effective drug treatments is research. Although there have been anti-PVR drug research reports, but side effects of these drugs is relatively large or relatively short half-life, therefore, seek to eye tissues toxic side effects and long half-life of the drug to combat PVR has important clinical significance. Suramin inhibit RPE cells and glial cell proliferation and migration, and participate in cell signaling role. In recent years, at home and abroad suramin RPE cells in vitro inhibition studies have been reported, but the prevention and treatment of traumatic PVR studies have not been reported. In this study, through the use of autologous platelet rich plasma intravitreal injection, creating a viable traumatic PVR rabbit model, while intravitreal injection of different concentrations of suramin. Double-antibody sandwich ELISA and radioimmunoassay were detected in five groups vitreous humor of EGF and TNF-α levels were observed traumatic PVR model group and the experimental group fundus and retinal pathological changes, which explore the prevention of PVR suramin mechanism of action for the future to provide a theoretical basis for clinical application. Methods: 40 healthy New Zealand white rabbits, of either sex, weighing 2.5 ~ 3.2kg. Using intravitreal injection of platelet rich plasma was prepared rabbit PVR model, randomly selected eight as a blank, and the remaining 36 Preparation of traumatic PVR model and randomly divided into 4 groups of 8. Model group were: 0.1ml saline intravitreal injection once; experimental group 1,2,3: intravitreal concentrations were one-time injection of 0.1ml 40mg/ml, 60mg/ml and 80mg/ml suramin. 1,3,7,14,21,28 respectively after the first day at the fully dilated using slit lamp microscope and direct ophthalmoscope to observe and record the wound, cornea, anterior chamber and vitreous retinal changes, reference Fastenberg rating criteria grading, and make eye fundus photography and B-ultrasound, using double-antibody sandwich ELISA and radioimmunoassay methods were used to detect the vitreous humor of EGF and TNF-α levels. Experimental data using SPSS13.0 statistical software for statistical analysis, PVR grade rank sum test case, P lt; 0.05 as significant criteria. Vitreous samples taken immediately after removal of the eye, retinal tissue samples taken near the wound routine HE staining, microscopy and photographed. Results: 1 with a slit lamp microscope, ophthalmoscope vitreoretinal changes observed in accordance Fastenberg rating criteria records. First day experimental group 1,2,3 1,3,7 proliferative vitreoretinal relatively slow, compared with the model group level hyperplasia, no statistically significant difference (P gt; 0.05). After the first 14 days, the proliferation of experimental group 3 level significantly lower than the model group, both of which had significant differences (Kruskal-Wallis P lt; 0.05), among other groups had no significant difference. 21, 28 days after the experimental group 1,2,3 proliferation levels were lower than the average model group, compared with the model group were significantly different (rank sum test P lt; 0.05). Experimental group 2,3 proliferation level is below the average experimental group 1, with the experimental group, there was a significant difference (rank test P lt; 0.05). Comparison between the experimental groups 2 and 3 were no significant differences (Kruskal-Wallis P gt; 0.05). Histological examination, suramin experiment three groups were not found significant morphological changes of the retina. 2 for the first 28 days, five groups of vitreous TNF-α and EGF levels were compared. Experimental group 1,2,3 vitreous cavity in TNF-α and EGF levels were lower than the model group, there was a significant difference (P lt; 0.01). Experimental group 1,2,3 vitreous cavity in TNF-α levels were higher than the control group, there were significant differences (P lt; 0.01 or p lt; 0.05). Vitreous cavity experimental group was higher than that of EGF blank group, there was a significant difference (P lt; 0.01). 2,3 vitreous cavity in experimental group and control group levels of EGF was no significant difference (P gt; 0.05). Experimental group 2,3 vitreous cavity in TNF-α and EGF levels were lower than the experimental one group, there was a significant difference (P lt; 0.01 or P lt; 0.05). 2,3 experimental group vitreous cavity TNF-α and EGF showed no significant difference (P gt; 0.05). 3. B-Results: 1st and 3rd days, the model group and the experimental group: intravitreal varying degrees of punctate, flocculent or thin ribbon echo wall echo is not closely linked with the ball. The first seven days, the model group and the experimental group: uneven performance of different lengths, running with irregular echo, or parallel to, bending, single-wall contact with the ball after a significant movement, there are multiple adhesion points After the motion was not significant, most do not connect with the optic nerve. On day 14, the model group: glass body in different shapes thick echogenic strip, connected with the optic nerve; experimental groups: vitreous cavity could be detected in the form of irregular hyperechoic spot, not connected with the wall of the eye, there are apparent after exercise. The first 21 days, the model group: vitreous cavity could be detected and gathered into a piece of echogenic spots and stripes hyperechoic band of light, a single contact with the wall of the eye significantly after exercise; experimental groups: see massive or vitreous membrane and a small amount of ribbon-like echo echo echo with small irregular walk the line, not connected with the wall of the eye, there are clear after the campaign. The first 28 days, the model group: glass body curved echogenic band, connected to the wall with the ball or strip connected to the optic nerve, turning the eye, the light with a mild tremor or showed a \, both ends connected to the sides of the serrated edge; experimental groups: vitreous cavity could be detected and uneven in hyperechoic band of light is not connected with the wall of the eye. Conclusion: With prolonged, PVR model group hyperplasia developed to more serious level; suramin experimental group hyperplasia with increasing concentration significantly reduced. Lamine said Ming Su inhibition in traumatic PVR and time and concentration; 2. Suramin experimental group intravitreal EGF, TNF-α levels significantly lower than the model group; description cytokines in the pathogenesis of traumatic PVR plays an important role, while suramin can effectively inhibit rabbit traumatic PVR occurrence and development; 3. morphological said Ming Su Lamine intravitreal injection safety, to maintain efficacy for a long time, no significant side effects on the retina.
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