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Samuel K. S. Chiang, Tim T. Lam; Post-Treatment at 12 or 18 Hours with 3-Aminobenzamide Ameliorates Retinal Ischemia–Reperfusion Damage. Invest. Ophthalmol. Vis. Sci. 2000;41(10):3210-3214.
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purpose. The window of protection afforded by 3-aminobenzamide (3-ABA), a
poly-(ADP-ribose) polymerase (PARP) inhibitor, against apoptotic loss
of inner retinal elements after ischemia–reperfusion insult in rats
methods. Ischemia–reperfusion injury to the retinas in albino Lewis rats was
induced by elevated intraocular pressure (IOP) through cannulation of
the anterior chamber with a needle connected to a saline column
delivering a pressure of 110 mm Hg. The ischemic period was held at 60
minutes, and reperfusion was established immediately afterward.
3-Aminobenzamide (3-ABA) was administered intravitreally at 0, 4, 8,
12, 18, or 24 hours after reperfusion and its effect evaluated by
morphology and morphometry of the inner retinas at 7 days after
reperfusion. Immunohistochemistry of poly-(ADP-ribose), a product of
PARP activity, and Western blot analysis for PARP were performed on
retinas at 0, 4, 8, 12, 18, and 24 hours after reperfusion.
results. Morphology and morphometry showed significantly better preserved inner
retinas in animals receiving 3-ABA between 12 and 18 hours after
reperfusion. Immunohistochemical study of poly-(ADP-ribose) showed
elevated levels at the retinal ganglion cell layer and the inner
nuclear layer at 12 and 18 hours after reperfusion. Western blot
analysis of PARP showed a notable increase in the 116-kDa band (PARP)
from 4 to 18 hours after reperfusion.
conclusions. Administration of 3-ABA at 12 or 18 hours after ischemia, when there
was accumulation of poly-(ADP-ribose) in the inner retina,
significantly ameliorated retinal ischemia–reperfusion injury. These
findings, together with earlier reports from our laboratory, are
consistent with a late and pivotal role of PARP in apoptotic loss of
inner retinal elements after ischemia–reperfusion insult to the
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