ANALYSIS OF LOCALIZATION OF ADULT T-CELL LEUKEMIA-DERIVED FACTOR IN THE TRANSIENT ISCHEMIC RAT RETINA AFTER TREATMENT WITH OP-1206 ALPHA-CD, A PROSTAGLANDIN E(1) ANALOG
M. Yamamoto et al., ANALYSIS OF LOCALIZATION OF ADULT T-CELL LEUKEMIA-DERIVED FACTOR IN THE TRANSIENT ISCHEMIC RAT RETINA AFTER TREATMENT WITH OP-1206 ALPHA-CD, A PROSTAGLANDIN E(1) ANALOG, The Journal of histochemistry and cytochemistry, 45(1), 1997, pp. 63-70
Prostaglandin E(1) (PGE(1)) is commonly used in therapy for obstructiv
e diseases, including ischemic retinopathy, in which pathogenetic reac
tive oxygen intermediates are responsible. However, the mechanism(s) o
f PGE(1) in reducing tissue damage is still unclear. Adult T-cell leuk
emia-derived factor/human thioredoxin (ADF) is induced by oxidative st
resses and has protective activity against oxidative cellular injury.
To evaluate the possible involvement of ADF in the tissue-protective e
ffect of PGE(1), we analyzed ADF expression immunohistochemically usin
g a rat transient retinal ischemia model. Rats were treated orally wit
h 300 mu g/kg/day OP-1206 alpha-cyclodextrin clathrate (OP-1206), a st
able PGE(1) analogue, for 14 days after photodynamic retinal vascular
thrombosis by rose Bengal. Rats without any OP-1206 treatment were use
d as controls. In the OP-1206-treated rats, minimal retinal atrophy du
e to ischemia/reperfusion was observed histologically up to 14 days, w
hereas in the non-treated rats the inner layer of the retina became ma
rkedly atrophic. In parallel with the histological change, after 14 da
ys following thrombosis ADF immunoreactivity was preserved on retinal
pigment epithelial cells in the OP-1206-treated rats, whereas it was d
iminished in the non-treated rats. These findings suggest an important
role for ADF in the OP-1206-dependent suppression of retinal tissue d
amage caused by oxidative insult.