Purchase this article with an account.
Yasuko Hasebe, Lauren R. Thomson, C. Kathleen Dorey; Pentoxifylline Inhibition of Vasculogenesis in the Neonatal Rat Retina. Invest. Ophthalmol. Vis. Sci. 2000;41(9):2774-2778.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
purpose. The zeta isozyme of protein kinase C (PKC) is essential for activation
of the transcription factor nuclear factor (NF)κB and transcription
of vascular endothelial growth factor (VEGF). This study examined the
antiangiogenic potential of an existing drug, pentoxifylline (PTX),
which inhibits PKC-dependent activation of NFκB and is reported to
prevent hypoxia-induced expression of VEGF.
methods. Neovascularization was induced by maintaining neonatal rats for 10 full
days in 80% oxygen, interrupted daily by 30 minutes in room air
followed by a progressive return to 80% oxygen. On experimental day
11, they were placed in room air until they were killed on day 17.
Daily intraperitoneal injections of PTX in saline (25 or 75 mg/kg per
day), or saline alone, were administered from day 6 through day 16.
Retinal neovascularization was scored, and avascular areas (AVAs) were
measured in ADPase stained retinas.
results. PTX inhibited radial extension of retinal vessels, causing increases in
AVA of 65% (P < 0.01) and 33% (P <
0.15) at the lower and upper doses, respectively. A significant
increase in mean neovascular score was seen at the lower dose
(P < 0.0001), but analysis of variance indicated that
neovascularization was strongly and positively influenced by the AVA
(P < 0.0001) and only weakly stimulated by PTX
(P < 0.05).
conclusions. Systemic PTX significantly inhibited VEGF-mediated retinal
vasculogenesis, but was not effective in reducing neovascularization in
the oxygen-exposed neonatal rat.
This PDF is available to Subscribers Only