چکیده:
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 excess activation of M1 microglia along with neuroinflammation are 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 lectins 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 injection of Amyloid-β1-42 peptide (Aβ) following 1, 5 or 10 μg Gal-1treatment for 14 days. Learning and memory abilities were estimated using the Morris water maze. Then, hippocampal samples were collected from rats, and the expression of M1 and M2 microglial markers was measured. The levels of inflammatory cytokines and the neuronal injury were also evaluated.
Results: At doses of 5 and 10 μg, Gal-1 exerted an effect on improving the Aβ-induced learning and memory impairments in rats (P<0.05, vs. Aβ group). Subsequently, Gal-1 efficaciously regulated microglial polarization, which evidenced by upregulating the expression of M2 microglial markers (P<0.01, vs. Aβ group) while downregulating M1 microglial markers (P<0.05, vs. Aβ group) and therefore contributed to decreasing the secretion of proinflammatory factors (P<0.01, vs. Aβ group) but increasing the production of anti-inflammatory factors (P<0.01, vs. Aβ group) as well as attenuating neuronal damage(P<0.01, vs. Aβ group) mediated by Aβ.
Conclusions: Gal-1 may exert neuroprotective effects by shifting microglia from the M1 phenotype to the M2 phenotype, which is beneficial for alleviating neuroinflammation, and it might be a potential agent to prevent AD-like neurodegeneration.
Methods: Male Sprague-Dawley rats received a single intracerebroventricular injection of Amyloid-β1-42 peptide (Aβ) following 1, 5 or 10 μg Gal-1treatment for 14 days. Learning and memory abilities were estimated using the Morris water maze. Then, hippocampal samples were collected from rats, and the expression of M1 and M2 microglial markers was measured. The levels of inflammatory cytokines and the neuronal injury were also evaluated.
Results: At doses of 5 and 10 μg, Gal-1 exerted an effect on improving the Aβ-induced learning and memory impairments in rats (P<0.05, vs. Aβ group). Subsequently, Gal-1 efficaciously regulated microglial polarization, which evidenced by upregulating the expression of M2 microglial markers (P<0.01, vs. Aβ group) while downregulating M1 microglial markers (P<0.05, vs. Aβ group) and therefore contributed to decreasing the secretion of proinflammatory factors (P<0.01, vs. Aβ group) but increasing the production of anti-inflammatory factors (P<0.01, vs. Aβ group) as well as attenuating neuronal damage(P<0.01, vs. Aβ group) mediated by Aβ.
Conclusions: Gal-1 may exert neuroprotective effects by shifting microglia from the M1 phenotype to the M2 phenotype, which is beneficial for alleviating neuroinflammation, and it might be a potential agent to prevent AD-like neurodegeneration.
نوع مطالعه: Original |
موضوع مقاله:
Cellular and molecular Neuroscience
دریافت: 1402/8/9 | پذیرش: 1403/1/28
دریافت: 1402/8/9 | پذیرش: 1403/1/28
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