Electroacupuncture pretreatment ameliorates cerebral ischemia/reperfusion injury by inhibiting the miR-124/NF-κB/Fas signaling pathway

Background The mechanism of electroacupuncture (EA) pretreatment for cerebral ischemia-reperfusion injury (CIRI) is unclear. This study aimed to investigate whether EA pretreatment attenuates CIRI through the miR-124/nuclear factor kappa B (NF-κB)/Fas signaling pathway. Methods Following 7 days of EA pretreatment at Baihui (GV20), Fengfu (GV16), and Dazhui (GV14), CIRI rats were established. Neuroprotection was assessed using modified neurological severity score (mNSS), 2,3,5-triphenyltetrazolium chloride staining, and terminal deoxynucleotidyl transferase dUTP nick end labeling staining. Neuronal ultrastructure was examined by electron microscopy. Immunofluorescence staining revealed pNF-κB and Fas expression patterns. Western blotting and real-time quantitative PCR were employed to quantify miR-124, NF-κB repressing factor (NKRF), pNF-κB/NF-κB ratio, Fas, FasL, fas-associated protein with death domain (FADD), caspase-3, and caspase-8 in the cerebral cortex. Results EA pretreatment reduced cerebral infarction volume, alleviated mNSS and cortical neuronal apoptosis. Moreover, EA pretreatment downregulated miR-124, pNF-κB/NF-κB/Fas, FasL, FADD levels and increased NKRF expression. The effect of EA pretreatment was enhanced by miR-124 inhibitor. Conclusion These findings suggest that EA pretreatment attenuated neuronal apoptosis through suppression of the miR-124/NF-κB/Fas signaling pathway in CIRI.