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

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.

Keywords::

• Cerebral ischemia
• paclitaxel
• neuroprotection
• c-Jun N-terminal kinase 3 (JNK3)
• Caspase-3

Acknowledgments

The authors wish to thank Yuan’s laboratory (Department of Chemistry, Yunnan Normal University) for offering paclitaxel.

Declaration of interest

This work is supported by the National Natural Science Foundation of China Grant (No. 81171075), Natural Science Foundation of the Jiangsu Higher Education Institutions of China (No. 08KJB180010, 11KJB310012, 09KJA180006), Foundation of Xuzhou Medical College (No. 2010KJZ13), and A Project Funded by the Priority Academic Program Development of Jiangsu Higher Education Institution.