MiRNA‐124 has been considered to play a significant role in the formation of memory and a variety of neurodegenerative diseases. In this study, the aim is to verify whether miRNA‐124 is involved in memory impairment induced by d‐galactose, and explore the underlying neuroprotective mechanism. The results revealed that rapid administration of d‐galactose (1000 mg/kg subcutaneously) in mice caused memory impairments, as determined by Novel Object Recognition test, Morris Water Maze test, and histological assessments. MiRNA‐124 agomir is stereotactic injected into hippocampus, thus alleviated memory impairment induced by d‐galactose and reversed the neural damage and neuroinflammation. Furthermore, the results of molecular biological analysis and immunohistochemistry revealed that miRNA‐124 markedly reduced neuroinflammation induced by d‐galactose through polarization of microglia as determined by detection of ionized calcium binding adapter molecule 1 (Iba‐1), inducible nitric oxide synthase (iNOS) and arginase‐1(Arg‐1), which also downregulated inflammatory mediators, including interleukin‐1β (IL‐1β) and tumor necrosis factor‐α (TNF‐α), and upregulated IL‐4 and IL‐10. Hence, taken together, the results of the present study suggested that miRNA‐124 showed a significant negative correlation with memory impairment and neuroinflammation induced by d‐galactose rapidly, possibly via polarization of microglia from M1 to M2. It is possible that miRNA‐124 can be used as a new target for the pathogenesis of memory impairment, including age‐associated neurodegenerative diseases such as Alzheimer's disease.
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