[논문]Polydeoxyribonucleotide (defibrotide) protects against post-ischemic behavioral, electroencephalographic and neuronal damage in the gerbil

Sala, Mariaelvina; Leone, Maria Primula; Lampugnani, Paola; Matturri, Luigi; Gori, Enzo

doi:10.1016/S0014-2999(97)83040-3

Polydeoxyribonucleotide (defibrotide) protects against post-ischemic behavioral, electroencephalographic and neuronal damage in the gerbil

European journal of pharmacology, v.328 no.2/3, 1997년, pp.143 - 152

Sala, Mariaelvina (Institute of Pharmacology, Faculty of Mathematical, Physical and Natural Sciences, University of Milan, Via Vanvitelli 32) , Leone, Maria Primula (Institute of Pharmacology, Faculty of Mathematical, Physical and Natural Sciences, University of Milan, Via Vanvitelli 32) , Lampugnani, Paola (Institute of Pharmacology, Faculty of Mathematical, Physical and Natural Sciences, University of Milan, Via Vanvitelli 32) , Matturri, Luigi (Department of Pathology, IRCCS Policlinical Hospital, University of Milan, Milan, Italy) , Gori, Enzo (Institute of Pharmacology, Faculty of Mathematical, Physical and Natural Sciences, University of Milan, Via Vanvitelli 32)

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AbstractThe effectiveness of defibrotide, a single-stranded polydeoxyribonucleotide compound, in preventing damage caused by cerebral ischemia was studied. Global ischemia was induced in anesthetized gerbils by bilateral carotid artery occlusion for 10 min. Defibrotide (100 mg/kg) or saline was injected, i.v., immediately after reperfusion. The following parameters were evaluated simultaneously: (1) electroencephalographic (EEG) spectral power, recorded before, during and after the ischemic period; (2) body temperature, monitored with a rectal thermistor probe after reperfusion for 120 min; (3) spontaneous motility, evaluated through a photocell system and quantified in terms of total distance travelled in 30 min, 1 h after recirculation and at periods over 15 days; (4) mnemonic functions assessed by passive avoidance test from 3 to 15 days after ischemia; (5) histological examination, 7 days after reperfusion, counting CA1 hippocampal neuronal cells. The ischemia-induced complete flattening of spectral power was significantly reversed (P<0.01) by post-ischemic treatment with defibrotide between 30 and 90 min after ischemia. A complete recovery of total EEG spectral power was seen in the defibrotide group at 6 h and the saline ischemic group at 1 day. Seven days after bilateral carotid occlusion, there was a significant decrease in spectral power (−70%±6) together with a loss of the number of CA1 cells in the saline ischemic group (−64%). Treatment with defibrotide significantly protected against the decrease in spectral power (−30%±7) and cell loss (−9%). Finally, the number of animals found to be protected against the ischemia-induced flattening was significantly larger for defibrotide-treated gerbils than for saline-treated animals throughout the experiment except for the third day. Body temperature was significantly decreased only at 30 min after reperfusion in both ischemic and sham-operated groups. Defibrotide reduced ischemia-induced hypermotility but only 6 h after the insult. The ischemia-induced impairment of memory was partially reversed within 3 days in the defibrotide-treated animals and fully reversed within 7 days in the defibrotide group and 15 days in the saline group. Our results demonstrate that defibrotide, even when administered after the post-ischemic period, possesses anti-ischemic properties. The mechanism by which defibrotide protects the ischemic reperfused brain is still largely unknown. However, a neuroprotection via adenosine A1 and A2 subtype receptor interaction can be put forward.

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Polydeoxyribonucleotide (defibrotide) protects against post-ischemic behavioral, electroencephalographic and neuronal damage in the gerbil

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