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Li S, Wang Y, Li J, Deng L, Dong Y. Effect of Galectin-1 on Classical Microglial Activation, Neuroinflammation, and Neuronal Damage in Rats Exposed to Amyloid-β Peptide. BCN 2026; 17 (2) :275-284
URL: http://bcn.iums.ac.ir/article-1-2818-fa.html

Introduction: Microglia-mediated neuroinflammation is one of the most striking hallmarks of Alzheimer’s disease (AD). Emerging evidence indicates that microglia can be polarized into proinflammatory M1 or anti-inflammatory M2 phenotypes, and excessive activation of M1 microglia, along with neuroinflammation, is critically associated with the pathogenesis and progression of AD. The aim of the present study was to test the hypothesis that Galectin-1 (Gal-1), a member of endogenous β-galactoside-binding lectin family, may improve AD-related neuroinflammation and that the modulation of microglial polarization plays a role in this process. 
Methods: Male Sprague-Dawley rats received a single intracerebroventricular (i.c.v.) injection of amyloid-β1-42 peptide (Aβ) followed by 1, 5, or 10 μg Gal-1 for 14 days. Learning and memory abilities were estimated using the Morris water maze (MWM). Then, hippocampal samples were collected from the rats, and the expression of M1 and M2 microglial markers was measured. The levels of inflammatory cytokines and neuronal injury were also evaluated. 
Results: At doses of 5 and 10 μg, Gal-1 exerted a significant effect on improving Aβ-induced learning and memory impairments in rats (P<0.05, vs the Aβ group). Subsequently, Gal-1 efficaciously regulated microglial polarization, as evidenced by upregulating the expression of M2 microglial markers (P<0.01, vs the Aβ group) while downregulating M1 microglial markers (P<0.05, vs the Aβ group). This modulation contributed to decreasing the secretion of proinflammatory factors (P<0.01, vs the Aβ group) and increasing the production of anti-inflammatory factors (P<0.01, vs the Aβ group), as well as attenuating neuronal damage (P<0.01, vs the Aβ group) mediated by Aβ. 
Conclusion: Gal-1 may exert neuroprotective effects by shifting microglia from the M1 phenotype to the M2 phenotype, which is beneficial for alleviating neuroinflammation. It may be a potential agent for preventing AD-like neurodegeneration.