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- W2028557994 abstract "<i>Background:</i> Inhibition of the c-Jun N-terminal kinase (JNK) pathway by the TAT-coupled peptide XG-102 (formerly D- JNKI1) induces strong neuroprotection in ischemic stroke in rodents. We investigated the effect of JNK inhibition in intracerebral hemorrhage (ICH). <i>Methods:</i> Three hours after induction of ICH by intrastriatal collagenase injection in mice, the animals received an intravenous injection of 100 µg/kg of XG-102. The neurological outcome was assessed daily and the mice were sacrificed at 6 h, 1, 2 or 5 days after ICH. <i>Results:</i> XG-102 administration significantly improved the neurological outcome at 1 day (p < 0.01). The lesion volume was significantly decreased after 2 days (29 ± 11 vs. 39 ± 5 mm<sup>3</sup> in vehicle-treated animals, p < 0.05). There was also a decreased hemispheric swelling (14 ± 13 vs. 26 ± 9% in vehicle-treated animals, p < 0.05) correlating with increased aquaporin 4 expression. <i>Conclusions:</i> XG-102 attenuates cerebral edema in ICH and functional impairment at early time points. The beneficial effects observed with XG-102 in ICH, as well as in ischemic stroke, open the possibility to rapidly treat stroke patients before imaging, thereby saving precious time." @default.
- W2028557994 created "2016-06-24" @default.
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- W2028557994 date "2010-01-01" @default.
- W2028557994 modified "2023-09-26" @default.
- W2028557994 title "c-Jun N-Terminal Kinase Pathway Inhibition in Intracerebral Hemorrhage" @default.
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- W2028557994 doi "https://doi.org/10.1159/000306643" @default.
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