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Neuroprotection of paclitaxel against cerebral ischemia/reperfusion-induced brain injury through JNK3 signaling pathway

机译:紫杉醇通过JNK3信号通路对脑缺血/再灌注所致脑损伤的神经保护

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摘要

In this study, we investigated the neuroprotective effects of paclitaxel in transient cerebral ischemia and possible regulatory mechanism of these neuroprotection. Our data showed that paclitaxel can down-regulate the increased MLK3, JNK3, c-Jun, Bcl-2, and caspase-3 phosphorylation induced by ischemia injury. Cresyl violet staining and immunohistochemistry results demonstrated that paclitaxel had neuroprotective effect against ischemia/reperfusion-induced neuronal cell death. These results indicated that paclitaxel has neuroprotection in ischemic injury through JNK3 signaling pathway and provided a novel possible drug in therapeutics of brain ischemia.
机译:在这项研究中,我们研究了紫杉醇在短暂性脑缺血中的神经保护作用以及这些神经保护作用的可能调节机制。我们的数据显示紫杉醇可以下调缺血性损伤诱导的MLK3,JNK3,c-Jun,Bcl-2和caspase-3磷酸化水平的升高。甲酚紫染色和免疫组织化学结果表明紫杉醇对缺血/再灌注诱导的神经元细胞死亡具有神经保护作用。这些结果表明紫杉醇通过JNK3信号通路在缺血性损伤中具有神经保护作用,为脑缺血的治疗提供了新的可能药物。

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