망막의 허혈/재관류 손상에 대한 Betaxolol후처리의 신경보호 효과
Neuroprotective effect of betaxolol post-treatment in the ischemia/reperfusion model of the rat retina
망막 허혈 재관류 BETAXOLOL 신경보호 신경생물학;
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The key of glaucoma management is to lower intraocular pressure (IOP). Betaxolol, a β-adrenoceptor antagonist as well as calcium channel blocker is effective at lowering IOP having a protective effect against excitotoxicity. This study was performed to elucidate the neuroprotective property afforded by post-treatment with betaxolol (Betoptic-S^(�), 0.25%) against loss of inner retinal elements with ischemia/reperfusion insult in rats. Ischemia was induced in the rat retina by raising the intraocular pressure above the systolic blood pressure for 60 min. Betaxolol was applied topically 1 or 3 days after the reperfusion, and its effect was evaluated by morphology, morphometry, choline acetyltransferase (ChAT) and tyrosine hydroxylase (TH) immunoreactivity of retinas 7 days later. In non-treated eyes, the thickness of the inner plexiform layer (IPL) decreased markedly after a reperfusion period of both 3 and 7 days. Moreover, retinal ChAT and TH-positive cells had almost completely disappeared in the retina 7 days after reperfusion. The results show that the inner retinal layers are more susceptible to ischemia/reperfusion injury than the outer retinal layer. However, when the eyes were treated with betaxolol after ischemia/reperfusion injury, the retinal ChAT and TH immunoreactivity and the thickness of the IPL were significantly increased. These findings suggest that betaxolol is an efficient neuroprotective agent for the prevention of retinal cell damage induced by ischemic injury in rats, as well as a treatment of the retinal ischemic event.