miR-125a-5p inhibits NF-κB by negatively regulating TRAF2 to alleviate inflammatory injury in ischemic stroke rats

The expression of certain miRNAs are significantly associated with both inflammatory and ischemia-reperfusion (I/R) injury in ischemic stroke. In this study, we identified cerebral cortex miR-125a-5p via RNA sequencing, which showed significant enrichment in inflammatory pathways. Cerebral infarction volume and neurological deficits were evaluated using TTC staining, mNSS scoring, and the open field test. Nissl staining and TUNEL assays were used to assess cortical apoptosis. TRAF2, NIK, and p-NFκB levels in the cerebral cortex, as well as serum TNF-α, IL-1β, and IFN-γ concentrations, were measured by Western blot and ELISA. We found that TRAF2, a predicted target of miR-125a-5p, is linked to NF-κB pathway. Overexpression of miR-125a-5p reduced infarct volume, inhibited apoptosis and neurological deficits, and downregulate TRAF2, NIK and p-NF-κB in the cortex, along with TNF-α, IL-1β, and INF-γ in the serum of I/R rats. The miR-125a-5p negatively regulates TRAF2, alleviating inflammation-induced I/R injury by modulating the NF-κB pathway.