ArticleNan fang yi ke da xue xue bao = Journal of Southern Medical University2025
[High expression of miR-124 improves cognitive function of sleep-deprived rats by modulating the PI3K/AKT signaling pathway].
Article in Nan fang yi ke da xue xue bao = Journal of Southern Medical University, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- [MiR-124 ameliorates MK-801-induced anxiety-like behaviors in mice by promoting hippocampal neural stem cell proliferation and differentiation].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026Article
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesTo explore the molecular mechanism by which miR-124 affects cognitive function of sleep-deprived rats.
methodsFifty-four adult male SD rats were randomized into 6 groups (
resultsIn Morris water maze test, the SD rat models treated with miR-124 agomir showed a significantly shorter escape latency and fewer platform crossings with increased percentage of time and swimming distance in the fourth quadrant as compared with those in SD model group, while the rats treated with miR-124 antagomir exhibited worsened performance in the test. In the SD rat models, treatment with miR-124 agomir obviously lessened pathological changes in the hippocampus, while treatment with miR-124 antagomir significantly worsened the pathological changes. Compared with those in SD model group, the miR-124 agomir-treated rats showed an increased hippocampal expression of miR-124 with upregulated protein expressions of PI3K, p-AKT/AKT, and Bcl-2 and downregulated expressions of Bax and caspase-3 proteins, while rats treated with miR-124 antagomir showed significantly decreased hippocampal expression of miR-124 with lowered expressions of PI3K, p-AKT/AKT and Bcl-2 proteins and increased Bax and caspase-3 protein expressions.
conclusionsHigh expression of miR-124 alleviates SD-induced cognitive decline and neuronal apoptosis in rats by activating the PI3K/AKT signaling pathway.
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