title: Triamcinolone acetonide prevents enhancement of hypoxia-induced neuronal and inducible nitric oxide synthases in the retinas of rats with oxygen-induced retinopathy.
abstract: OBJECTIVE
  We investigated whether oxygen-induced retinopathy (OIR) results in changes in the protein expression of neuronal and inducible nitric oxide synthases (nNOS and iNOS, respectively) in rat model of OIR. In addition, we evaluated whether treatment of rats with triamcinolone acetonide (TA) prevents this response.
  
  
  METHODS
  To promote OIR, Sprague-Dawley rats were exposed to hyperoxia from postnatal day 2 (P2) to P14. They were then returned to normoxia after P15. TA was injected into the right vitreous of P15 rats, while saline was injected into the left vitreous. At P18 the expression of nNOS and iNOS was determined using Western blotting and immunostaining techniques in retinas obtained from control rats.
  
  
  RESULTS
  In P18 OIR rats, the abundance of nNOS and iNOS protein was significantly increased compared with controls. These increases were not observed in the retinas of rats treated with TA. The change in expression of nNOS and iNOS were specific to parvalbumin and glial fibrillary acidic protein-positive cells. Treatment with TA prevented the increased expression of nNOS and iNOS in all samples.
  
  
  CONCLUSIONS
  Hypoxia upregulates expression of nNOS and iNOS in OIR rat retinas, which is can be prevented by treatment with TA.
authors.affiliation: Department of Ophthalmology, Gyeongsang National University School of Medicine, Jinju, Korea.
authors.forename: Seong Jae
authors.initials: SJ
authors.lastname: Kim
authors.forename: In Young
authors.initials: IY
authors.lastname: Chung
authors.forename: Wan Sung
authors.initials: WS
authors.lastname: Choi
authors.forename: Young Hee
authors.initials: YH
authors.lastname: Kim
authors.forename: Ji Myong
authors.initials: JM
authors.lastname: Yoo
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D015153:Blotting, Western; D004195:Disease Models, Animal; D005260:Female; D005938:Glucocorticoids / Q000494:pharmacology; D000860:Hypoxia / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D007150:Immunohistochemistry; D009474:Neurons / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000096:biosynthesis*; D010100:Oxygen / Q000633:toxicity; D011247:Pregnancy; D011270:Pregnancy, Animal; D051381:Rats; D017207:Rats, Sprague-Dawley; D012160:Retina / Q000378:metabolism* / Q000473:pathology; D012164:Retinal Diseases / Q000139:chemically induced / Q000473:pathology / Q000517:prevention & control*; D014222:Triamcinolone Acetonide / Q000494:pharmacology*
chemical_list: D005938:Glucocorticoids; D052247:Nitric Oxide Synthase Type II; C496318:Nos2 protein, rat; D014222:Triamcinolone Acetonide; D010100:Oxygen