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紫杉醇通过JNK3信号通路对脑缺血/再灌注诱导的脑损伤的神经保护作用。

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

作者信息

Qi Su-Hua, Zhao Hui, Gong Juan-Juan, Sun Fu-Mou, Yue Jun, Guan Qiu-Hua, Wang Min

机构信息

Research Center for Biochemistry and Molecular Biology and Provincial Key Laboratory of Brain Disease Bioinformation, Xuzhou Medical College , Xuzhou, P. R. China.

出版信息

J Recept Signal Transduct Res. 2011 Dec;31(6):402-7. doi: 10.3109/10799893.2011.621070. Epub 2011 Nov 7.

DOI:10.3109/10799893.2011.621070
PMID:22060185
Abstract

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.

摘要

在本研究中,我们探讨了紫杉醇在短暂性脑缺血中的神经保护作用及其神经保护的可能调控机制。我们的数据表明,紫杉醇可下调缺血损伤诱导的MLK3、JNK3、c-Jun、Bcl-2和caspase-3磷酸化水平升高。甲酚紫染色和免疫组化结果表明,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信号通路在缺血损伤中具有神经保护作用,并为脑缺血治疗提供了一种新的可能药物。

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