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Galectin-1 attenuates astrogliosis-associated injuries and improves recovery of rats following focal cerebral ischemia
被引:36
|作者:
Qu, Wen-Sheng
[1
]
Wang, Yi-Hui
[1
]
Ma, Jun-Fang
[1
]
Tian, Dai-Shi
[1
]
Zhang, Qiang
[1
]
Pan, Deng-Ji
[1
]
Yu, Zhi-Yuan
[1
]
Xie, Min-Jie
[1
]
Wang, Jian-Ping
[2
]
Wang, Wei
[1
]
机构:
[1] Huazhong Univ Sci & Technol, Dept Neurol, Tongji Hosp, Tongji Med Coll, Wuhan 430074, Peoples R China
[2] Zhengzhou Univ, Dept Neurol, Affiliated Hosp 5, Zhengzhou, Peoples R China
基金:
中国国家自然科学基金;
关键词:
astrogliosis;
cerebral ischemia;
function recovery;
galectin-1;
neuronal apoptosis;
CYCLE PROTEIN EXPRESSION;
INDUCED PROLIFERATION;
NEUROPROTECTIVE ROLE;
AXONAL REGENERATION;
FUNCTIONAL RECOVERY;
BRAIN ISCHEMIA;
SCAR FORMATION;
CELL-DEATH;
IN-VITRO;
ASTROCYTES;
D O I:
10.1111/j.1471-4159.2010.07095.x
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:
P>Astrogliosis occurs after brain ischemia, and excessive astrogliosis can devastate the neuronal recovery. Previous reports show that galectin-1 (Gal-1) regulates proliferation of several cell types and plays an important role after nervous system injuries. Here, we found that expression of Gal-1 was remarkably up-regulated in activated astrocytes around ischemic infarct. Furthermore, under ischemic conditions either in vitro or in vivo, Gal-1 was found to inhibit the proliferation of astrocytes in a dose-dependent manner, attenuate astrogliosis and down-regulate the astrogliosis associated expression of nitric oxide synthase and interleukin-1 beta after the ischemia. All these changes were blocked by lactose, suggesting a lectin dependent manner of Gal-1's function. Moreover, 7-day Gal-1 treatment reduced apoptosis of neurons, decreased brain infarction volume and improved neurological function induced by the ischemia. Together, these findings indicate that through reducing astrogliosis related damages, Gal-1 is a potential therapeutical target for attenuating neuronal damage and promoting recovery of brain ischemia.
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页码:217 / 226
页数:10
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