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• W2896216926 abstract "Studies from our lab have indicated that stimulation of ETB receptors by IRL-1620 produced a marked functional recovery in a rat model of AD. Aβ-treated rats showed a significant impairment in spatial memory. The Aβ-induced cognitive impairment was significantly improved by IRL-1620 treatment. IRL-1620 significantly decreased oxidative stress and increased VEGF and NGF expression in Aβ animals. These effects were blocked by ETB receptor antagonist BQ788, confirming the involvement of ETB receptors. The mechanism by which IRL-1620 produced functional recovery is not known. Therefore, the purpose of this study is to determine the signaling pathways involved in the efficacy of IRL-1620 in Aβ-induced cognitive impairment. Rats were treated with Aβ1–40 in the lateral cerebral ventricles using stereotaxically implanted cannula and IRL-1620 was intravenously administered on day 8; experiments were performed on day15. Learning and memory behavior was assessed using the Morris water maze. Rats were sacrificed for estimation of brain apoptotic markers using western blot. Additionally, mouse brain were cultured, incubated for 24h with Aβ1-42, and treated with 1nM of IRL-1620 (1,3,5h). Thereafter, an MTT assay was performed to determine cell viability. In the Morris swim task, Aβ-induced cognitive impairment was significantly(p<0.001) improved by IRL-1620 treatment. The MTT assay of brain slices revealed a significant(p<0.05) increase in cell viability in the IRL-1620 group compared Aβ alone. PI3K and pAkt expression significantly increased (90 % and 139%, respectively) in IRL-1620 treated rats verses vehicle [F(4, 15)=35.52,p<0.0001]. Anti-apoptotic protein Bcl-2 expression was decreased (-48%) and pro-apoptotic protein Bax expression was increased (63%) in the vehicle-treated group compared to sham(p<0.0001). On the other hand, IRL-1620 treatment showed significantly(p<0.01) increased (66%) expression of Bcl-2 and decreased (-40%) expression of Bax. Results of the present study demonstrate that IRL-1620 improves memory deficit at least in part through a reduction in apoptosis. Stimulation of ETB receptors appears to initiate a signaling cascade resulting in the recruitment of PI3K and subsequent activation of Akt via phosphorylation, along with a reduction in pro-apoptotic marker. Present results support the idea that IRL-1620 may be capable of significantly reducing the progressive neurodegeneration associated with AD." @default.
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• W2896216926 date "2018-07-01" @default.
• W2896216926 modified "2023-10-16" @default.
• W2896216926 title "P4‐258: STIMULATION OF ET _B RECEPTORS BY IRL‐1620 IS ANTI‐APOPTOTIC AND SLOWS THE PROGRESSION OF ALZHEIMER'S DISEASE" @default.
• W2896216926 doi "https://doi.org/10.1016/j.jalz.2018.07.080" @default.
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