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本人已完成文章的写作，但是由于毕业在即，需要在明年3月份之前拿到accept，希望有人能够根据下述内容帮忙推荐接收几率高和审稿周期短的文章，非常感谢！ Vinpocetine has found wide application in the treatment of cerebral diseases, and it shows benefits especially in the treatment of stroke and epilepsy. However, it has the disadvantages of low bioavailability and cardiac toxicity. Studies have shown that vinpocetine derivatives with higher potency can be obtained through modification and screening. The aim of this study is to assess the pharmacodynamics of vinpocetine derivative VPK from such aspects as anti-cerebral ischemia, anti-epilepsy, inhibiting PDE1 and Na+ channel. The changes in the volume of cerebral infarction were examined after pharmacotherapy by employing rat model of cerebral ischemia reperfusion injury. PTZ-kindled SD rat and cynomolgus macaque epilepsy models were used to detect the latency, counts and duration of epilepsy, and to study the pharmacodynamic actions of VPK in vivo; the inhibitory effects of VPK on PDE1 and Na+ channel were also detected and its pharmacodynamic actions in vitro on stroke and epilepsy were expounded at the molecular level. With respect to its in vivo pharmacodynamic effects, VPK was significantly superior to vinpocetine and carbamazepine in inhibiting cerebral infarction caused by middle cerebral artery occlusion (MCAO), prolonging the latency of epilepsy, reducing the counts and duration of epilepsy, which showed dose-dependent effect. At the molecular level in vitro, the 50% inhibitory concentrations (IC50) of VPK and vinpocetine for PDE1 were 1.97 μM and 17.4 μM respectively, and IC50s for NaV1.1 were 0.013 μM and 0.25 μM respectively. The results above show that the pharmacodynamic effects of VPK are significantly superior to that of vinpocetine and carbamazepine.  VPK has higher potency than vinpocetine in the treatment of stroke and epilepsy, which suggests that it may become a new drug candidate which is more effective in the treatment of stroke and epilepsy. |
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