Neuroprotective effects of BayK8644 against ischemic neuronal death in vivo and in vitro

来源 :中国神经科学学会第九届全国学术会议暨第五届会员代表大会 | 被引量 : 0次 | 上传用户:vingf
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  Stroke is the leading cause of disability and the third cause of death in the world.Currently, underlying mechanisms of neuronal death induced by ischemic brain injury remain unclear and treatments for stroke are limited, mainly because of the short therapeutic window for stroke.Although Ca2+ very early plays critical role in neuronal death induced by brain ischemia, activation of L-type Ca2+ channel effectively triggers a group of genes required for neuronal survival and the currents mediated by L-type Ca2+ channel indeed decreased in CA1 neurons 24 h after forebrain ischemia.Previously we showed that L-type Ca2+ channel agonist, BayK8644 produced neuroprotective effects in oxygen-glucose deprivation (OGD) and forebrain ischemic animal models.In present study, by using these two models, we tested the extended therapeutic window of BayK8644 for treatment of ischemic brain injury and the involved mechanisms were also determined.
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