Journal
JOURNAL OF NEUROCHEMISTRY
Volume 116, Issue 2, Pages 217-226Publisher
WILEY
DOI: 10.1111/j.1471-4159.2010.07095.x
Keywords
astrogliosis; cerebral ischemia; function recovery; galectin-1; neuronal apoptosis
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Funding
- China National Funds for Distinguished Young Scientists [30725019]
- Key Project [81030021]
- National Natural Science Foundation of China [30800340, 30800341, 30971009, 30971007]
- Medical Research Project of Henan Province [WKJ-2007-2-031]
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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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