Abstract |
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-1β 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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Authors | Wen-Sheng Qu, Yi-Hui Wang, Jun-Fang Ma, Dai-Shi Tian, Qiang Zhang, Deng-Ji Pan, Zhi-Yuan Yu, Min-Jie Xie, Jian-Ping Wang, Wei Wang |
Journal | Journal of neurochemistry
(J Neurochem)
Vol. 116
Issue 2
Pg. 217-26
(Jan 2011)
ISSN: 1471-4159 [Electronic] England |
PMID | 21054390
(Publication Type: Comparative Study, Journal Article, Research Support, Non-U.S. Gov't)
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Copyright | © 2010 The Authors. Journal of Neurochemistry © 2010 International Society for Neurochemistry. |
Chemical References |
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Topics |
- Animals
- Astrocytes
(metabolism, pathology)
- Brain Ischemia
(drug therapy, metabolism)
- Cells, Cultured
- Disease Models, Animal
- Galectin 1
(biosynthesis, physiology, therapeutic use)
- Gliosis
(drug therapy, metabolism, pathology)
- Male
- Random Allocation
- Rats
- Rats, Wistar
- Recovery of Function
(physiology)
- Up-Regulation
(physiology)
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