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dc.contributor.authorEren, Burak
dc.contributor.authorKaracan, Murat
dc.contributor.authorÖnay-Uçar, Evren
dc.contributor.authorVahabova, Güney
dc.contributor.authorÖzcan, Tevhide Bilgen
dc.contributor.authorGüleç, İlker
dc.contributor.authorŞengelen, Aslıhan
dc.contributor.authorKaragöz-Güzey, Feyza
dc.date.accessioned2021-12-10T10:54:58Z
dc.date.available2021-12-10T10:54:58Z
dc.identifier.citationGüleç İ., Şengelen A., Karagöz-Güzey F., Önay-Uçar E., Eren B., Vahabova G., Karacan M., Özcan T. B. , "The calcimimetic R-568 attenuates subarachnoid hemorrhage-induced vasospasm through PI3K/Akt/eNOS signaling pathway in the rat model.", Brain research, cilt.1765, ss.147508, 2021
dc.identifier.issn0006-8993
dc.identifier.othervv_1032021
dc.identifier.otherav_5bf87610-ac04-42f3-bbb5-467ae77cc624
dc.identifier.urihttp://hdl.handle.net/20.500.12627/170832
dc.identifier.urihttps://doi.org/10.1016/j.brainres.2021.147508
dc.description.abstractCerebral vasospasm (CVS) causes mortality and morbidity in patients after subarachnoid hemorrhage (SAH). The mechanism and adequate treatment of CVS are still elusive. R-568 is a calcimimetic agent known to exert a vasodilating effect. However, there is no report on its vasodilator effect against SAH-induced vasospasm. In the present study, we investigated the therapeutic effect of R-568 on the SAH-induced CVS model in rats. Seventytwo adult male Sprague-Dawley rats were divided into 8 groups: sham surgery; SAH only; SAH + Vehicle, SAH + R-568; SAH + R-568 + Wortmannin (the PI3K inhibitor); SAH + Wortmannin; SAH + R-568 + Calhex-231 (a calcilytic agent); SAH + Calhex-231. SAH was induced by blood (0.3 mL) given by intracisternal injection. R-568 (20 mu M) was administered intracisternal immediately prior to experimental SAH. Basilar arteries (BAs) were obtained to evaluate PI3K/Akt/eNOS pathway (immunoblotting) and morphological changes 48 h after SAH. Perimeters of BAs were decreased by 24.1% in the SAH group compared to the control group and the wall thickness was increased by 75.3%. With R-568 treatment, those percentages were 9.6% and 29.6%, respectively, indicating that vasospasm was considerably improved when compared with the SAH group (P < 0.001 in both). While p-PI3K/PI3K and p-Akt/Akt ratio and eNOS protein expression were markedly decreased in the SAH rats, treatment with R-568 resulted in a significant increase in these levels. The beneficial effects of R-568 were partially blocked in the presence of Calhex-231 and completely blocked in the presence of Wortmannin. Herein, we found that treatment with R-568 would attenuate SAH-induced CVS through the PI3K/Akt/eNOS pathway and demonstrate therapeutic promise in CVS treatment following SAH.
dc.language.isoeng
dc.subjectSinirbilim ve Davranış
dc.subjectYaşam Bilimleri (LIFE)
dc.subjectNEUROSCIENCES
dc.titleThe calcimimetic R-568 attenuates subarachnoid hemorrhage-induced vasospasm through PI3K/Akt/eNOS signaling pathway in the rat model.
dc.typeMakale
dc.relation.journalBrain research
dc.contributor.department, ,
dc.identifier.volume1765
dc.identifier.startpage147508
dc.identifier.endpage147508
dc.contributor.firstauthorID2639949


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