Background: Tranilast has been clinically used for various allergic disease
s. Recently, it has also been found to inhibit excessive scarring in wound
healing processes. In this study, we examined the effects of tranilast on t
he treatment for experimental proliferative vitreoretinopathy (PVR). Method
s: Cultured rabbit conjunctival fibroblasts were injected intravitreously (
50 000 cells/eye) into the rabbit vitreous to induce experimental PVR. Imme
diately after that, tranilast (0.5-5 mg/ml, 0.1 ml/eye) was injected into t
he vitreous. Injection of vehicle solution was used as a negative control.
PVR was clinically evaluated by masked observers using ophthalmoscopy and g
raded into six stages: 0 (no PVR) to 5 (severe PVR). The amount of transfor
ming growth factor beta 1 (TGF-beta 1) in the vitreous was measured by ELIS
A method. Functional and morphological changes induced by 5 mg/ml tranilast
were sought by electroretinography, light microscopy, and electron microsc
opy on day 28. Results: The average stage of PVR in the eyes treated with t
ranilast (1 or 5 mg/ml) was significantly lower than that in the control gr
oup on days 14 and 28. There was no difference between the eyes treated wit
h low-dose tranilast (0.5 mg/ml) and the control group. The amount of TGF-b
eta 1 in the vitreous of tranilast-treated eyes was significantly lower tha
n in the control group. The morphological and functional studies did not sh
ow any deleterious effect of tranilast on the retinal function and morpholo
gy. Conclusion: Tranilast effectively inhibits the progression of PVR witho
ut showing apparent toxicity of the eye. This agent has therapeutic value f
or PVR.