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

被引:9
作者
Qi, Su-Hua [1 ,2 ]
Zhao, Hui [3 ,4 ]
Gong, Juan-Juan [1 ,2 ]
Sun, Fu-Mou [5 ]
Yue, Jun [1 ,2 ]
Guan, Qiu-Hua [1 ,2 ]
Wang, Min [6 ]
机构
[1] Xuzhou Med Coll, Res Ctr Biochem & Mol Biol, Xuzhou 221002, Peoples R China
[2] Xuzhou Med Coll, Prov Key Lab Brain Dis Bioinformat, Xuzhou 221002, Peoples R China
[3] Nanjing Med Univ, Nanjing Brain Hosp, Dept Neurol, Nanjing, Peoples R China
[4] Xuzhou Cent Hosp, Dept Neurol, Xuzhou, Peoples R China
[5] China Pharmaceut Univ, Sch Pharmaceut Sci, Nanjing 210009, Peoples R China
[6] China Pharmaceut Univ, Sch Life Sci & Biotechnol, Nanjing 210009, Peoples R China
基金
中国国家自然科学基金;
关键词
Cerebral ischemia; paclitaxel; neuroprotection; c-Jun N-terminal kinase 3 (JNK3); Caspase-3; RAT HIPPOCAMPAL CA1; MAP KINASES; C-JUN; APOPTOSIS; ISCHEMIA; NEURONS; TRANSDUCTION; INHIBITOR; TAXOL;
D O I
10.3109/10799893.2011.621070
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
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.
引用
收藏
页码:402 / 407
页数:6
相关论文
共 21 条
[1]   Signal transduction by the JNK group of MAP kinases [J].
Davis, RJ .
CELL, 2000, 103 (02) :239-252
[2]   MEKKs, GCKs, MLKs, PAKs, TAKs, and Tpls: Upstream regulators of the c-Jun amino-terminal kinases? [J].
Fanger, GR ;
Gerwins, P ;
Widmann, C ;
Jarpe, MB ;
Johnson, GL .
CURRENT OPINION IN GENETICS & DEVELOPMENT, 1997, 7 (01) :67-74
[3]   The neuroprotective action of SP600125, a new inhibitor of JNK, on transient brain ischemia/reperfusion-induced neuronal death in rat hippocampal CA1 via nuclear and non-nuclear pathways [J].
Guan, QH ;
Pei, DS ;
Zhang, QG ;
Hao, ZB ;
Xu, TL ;
Zhang, GY .
BRAIN RESEARCH, 2005, 1035 (01) :51-59
[4]  
Guibin L, 2003, J NEUROCHEM, V84, P347
[5]   Role of mitogen- and stress-activated kinases in ischemic injury [J].
Irving, EA ;
Bamford, M .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 2002, 22 (06) :631-647
[6]   A critical role of neural-specific JNK3 for ischemic apoptosis [J].
Kuan, CY ;
Whitmarsh, AJ ;
Yang, DD ;
Liao, GH ;
Schloemer, AJ ;
Dong, C ;
Bao, J ;
Banasiak, KJ ;
Haddad, GG ;
Flavell, RA ;
Davis, RJ ;
Rakic, P .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2003, 100 (25) :15184-15189
[7]  
LOWRY OH, 1951, J BIOL CHEM, V193, P265
[8]  
Maroney AC, 1998, J NEUROSCI, V18, P104
[9]   MORPHOLOGICAL ALTERATIONS IN DORSAL-ROOT GANGLION NEURONS AND SUPPORTING CELLS OF ORGANOTYPIC MOUSE SPINAL CORD-GANGLION CULTURES EXPOSED TO TAXOL [J].
MASUROVSKY, EB ;
PETERSON, ER ;
CRAIN, SM ;
HORWITZ, SB .
NEUROSCIENCE, 1983, 10 (02) :491-509
[10]  
Michaelis ML, 1998, J NEUROCHEM, V70, P1623