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Galectin-1 attenuates astrogliosis-associated injuries and improves recovery of rats following focal cerebral ischemia.

Journal of Neurochemistry

Animals, Astrocytes, metabolism, pathology, Brain Ischemia, drug therapy, Cells, Cultured, Disease Models, Animal, Galectin 1, biosynthesis, physiology, therapeutic use, Gliosis, Male, Random Allocation, Rats, Rats, Wistar, Recovery of Function, Up-Regulation

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      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. © 2010 The Authors. Journal of Neurochemistry © 2010 International Society for Neurochemistry.

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      21054390
      10.1111/j.1471-4159.2010.07095.x

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