Electroacupuncture Improves Neuroinflammatory Injury in CPSP Rats by Inhibiting LncRNA MEG3-Mediated Wnt/β-Catenin Signaling Pathway

Background Electroacupuncture (EA) therapy has shown significant effects in alleviating central post-stroke pain (CPSP). However, current research on the mechanisms by which EA relieves CPSP is insufficient. This study explores the role of EA in improving central nervous system inflammation in CPSP rats. Methods The CPSP rat model was established by injecting collagenase IV into the right ventral posterolateral nucleus of the thalamus. After modeling, rats received EA treatment at DU20 and ST36 acupoints, administered every other day for a total of 8 sessions. LncRNA MEG3 was knocked down or over-expressed by adeno-associated virus vectors delivery in vivo in rat brain befor modeling. Mechanical and thermal pain thresholds were measured to assess the hypersensitivity to pain of rats. Immunofluorescence, Nissl staining and ELISA were respectively used to assess the levels of LncRNA MEG3 and GFAP, neuronal injury, and the levels of SP, TNF-α, IL-1β and IL-6. The levels of LncRNA MEG3, Wnt3a, β-catenin and GFAP were detected by qRT-PCR or Western blot . Results EA inhibits the expression of LncRNA MEG3 and neuroinflammatory injury in the brain tissue of CPSP rats, improving hyperalgesia symptoms in CPSP rats. Overexpression of MEG3 weakened the inhibitory effect of EA on the Wnt/β-catenin pathway in the brain's VPL region, exacerbating pain hypersensitivity and neuroinflammatory damage in the brain hemorrhage regions of CPSP rats. Suppressing the expression of MEG3 in the brain tissue of CPSP rats produced a therapeutic effect similar to that of EA intervention. Conclusion EA improves central nervous inflammation injury in CPSP rats by regulating the LncRNA MEG3-mediated Wnt/β-catenin signaling pathway.