title: The effect of tranilast on experimental proliferative vitreoretinopathy.
abstract: BACKGROUND
  Tranilast has been clinically used for various allergic diseases. Recently, it has also been found to inhibit excessive scarring in wound healing processes. In this study, we examined the effects of tranilast on the treatment for experimental proliferative vitreoretinopathy (PVR).
  
  
  METHODS
  Cultured rabbit conjunctival fibroblasts were injected intravitreously (50000 cells/eye) into the rabbit vitreous to induce experimental PVR. Immediately after that, tranilast (0.5-5 mg/ml, 0.1 ml/eye) was injected into the vitreous. Injection of vehicle solution was used as a negative control. PVR was clinically evaluated by masked observers using ophthalmoscopy and graded into six stages: 0 (no PVR) to 5 (severe PVR). The amount of transforming growth factor beta1 (TGF-beta1) in the vitreous was measured by ELISA method. Functional and morphological changes induced by 5 mg/ml tranilast were sought by electroretinography, light microscopy, and electron microscopy on day 28.
  
  
  RESULTS
  The average stage of PVR in the eyes treated with tranilast (1 or 5 mg/ml) was significantly lower than that in the control group on days 14 and 28. There was no difference between the eyes treated with low-dose tranilast (0.5 mg/ml) and the control group. The amount of TGF-beta1 in the vitreous of tranilast-treated eyes was significantly lower than in the control group. The morphological and functional studies did not show any deleterious effect of tranilast on the retinal function and morphology.
  
  
  CONCLUSIONS
  Tranilast effectively inhibits the progression of PVR without showing apparent toxicity of the eye. This agent has therapeutic value for PVR.
authors.affiliation: Department of Ophthalmology, Faculty of Medicine, Kyushu University, Fukuoka, Japan. ito@eye.med.kyushu-u.ac.jp
authors.forename: S
authors.initials: S
authors.lastname: Ito
authors.forename: T
authors.initials: T
authors.lastname: Sakamoto
authors.forename: Y
authors.initials: Y
authors.lastname: Tahara
authors.forename: Y
authors.initials: Y
authors.lastname: Goto
authors.forename: K
authors.initials: K
authors.lastname: Akazawa
authors.forename: T
authors.initials: T
authors.lastname: Ishibashi
authors.forename: H
authors.initials: H
authors.lastname: Inomata
mesh_terms: D000818:Animals; D002478:Cells, Cultured; D004195:Disease Models, Animal; D018450:Disease Progression; D004596:Electroretinography; D004797:Enzyme-Linked Immunosorbent Assay; D005347:Fibroblasts / Q000502:physiology; D006634:Histamine H1 Antagonists / Q000494:pharmacology*; D011817:Rabbits; D012160:Retina / Q000187:drug effects* / Q000378:metabolism / Q000648:ultrastructure; D016212:Transforming Growth Factor beta / Q000378:metabolism; D016896:Treatment Outcome; D018630:Vitreoretinopathy, Proliferative / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D014822:Vitreous Body / Q000187:drug effects* / Q000378:metabolism / Q000648:ultrastructure; D062367:ortho-Aminobenzoates / Q000494:pharmacology*
chemical_list: D006634:Histamine H1 Antagonists; D016212:Transforming Growth Factor beta; D062367:ortho-Aminobenzoates; C012293:tranilast