To verify whether long non-coding RNA (lncRNA) MALAT1 participates in neuronal
injury after cerebral infarction, and to explore the underlying mechanism of MALAT1. Methods: An in vitro
cellular model of cerebral infarction was established by oxygen-glucose deprivation/reoxygenation (OGD/R).
Cell viability was measured using the CCK-8 assay. Flow cytometry was applied to analyze the cell apoptosis
rate. Enzyme-linked immunosorbent assay (ELISA) was used to detect the levels of inflammation-related factors
including tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6). Western blot was performed to detect the
expression of apoptosis-related proteins (Bax, Bcl-2). RT-qPCR was adopted to quantify the expression levels of
MALAT1 and miR-125b. Dual-luciferase reporter assay was used to verify the regulatory interaction between
MALAT1 and miR-125b. Co-immunoprecipitation (Co-IP) was utilized to detect the binding between P35 and
CDK5. Results: The OGD/R cell model was successfully established. Compared with the Control group,
MALAT1 expression was significantly downregulated in the OGD/R group. After overexpression of MALAT1,
neuronal viability was increased, the apoptosis level was decreased; the levels of TNF-α, IL-6, Bax and P25 were
markedly reduced, whereas the levels of Bcl-2 and P35 were significantly elevated. Further experiments
demonstrated that MALAT1 negatively regulated miR-125b expression. The addition of miR-125b mimic
reversed the protective effects of MALAT1 overexpression in OGD/R-treated neurons; meanwhile, the
expression of P35 was further increased and P25 expression was further decreased. Conclusion: MALAT1
ameliorates cerebral infarction-induced neuronal injury by inhibiting miR-125b to regulate the P35-CDK5
pathway.
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