MicroRNA‐429 Inhibits Microglial Inflammation by Targeting <i>IKKβ</i> Through the NF‐κB Pathway

This study was designed to explore the specific mechanism of miR-429 in neuroinflammation of TS, to provide a theoretical basis for the etiology of TS and new targets for future treatment. Male SD rats were randomly divided into the normal control (CON) group and the Tourette syndrome (TS) group. The activation of microglia in the striatum was detected by immunohistochemistry and the concentration of interleukin (IL)-6 in the brain was measured by ELISA. The expression of miR-429 in brains was detected by quantitative real-time PCR (qPCR). Human microglia clone 3 (HMC3) cells were transfected, respectively, with double-stranded inactive miRNA; miR-429 mimics; miR-429 inhibitors. The levels of miR-429 and <i>IKKβ</i> mRNA were detected by qPCR. The expression levels of IKKβ, NF-κBp65 b, and IL-6 proteins were detected by western blot. MiR-429 and <i>IKKβ</i> targeted binding was verified by a double luciferase experiment. IL-6 in the brain of the TS rat group was higher than in the CON group. Furthermore, the relative expression of miR-429 in the TS group was several hundreds of times higher than in the CON group. The levels of IKKβ, NF-κBp65, and IL-6 protein in lipopolysaccharide (LPS)-induced microglia were lower in the miR-429 mimics group, but higher in the miR-429 inhibitor group, compared to those of the MiRNA negative control (miR-NC) group (<i>p</i> < 0.05). The miR-429 targeted <i>IKKβ</i> binding to regulate the NF-κB pathway and inhibit the release of pro-inflammatory factors, thus, controlling neuroinflammation in microglia, which may be the mechanism of action of miR-429 in TS.