To explore the protective effects of 6-shogaol(6-SH)against cerebral is chemia-reperfusion injury(CIRI)in rats,mo-lecular docking was utilized to investigate the spontaneous binding ability of 6-SH with microRNA-26a-5p(miRNA-26a-5P).Dual lu-ciferase reporter gene assays were employed to validate the targeted relationship between miRNA-26a-5p and death associated protein kinase 1(DAPK1).The CIRI rat model was induced using the suture method,with male SD rats randomly assigned to sham surgery,model,and 6-shogaol groups.Improved neurological function scoring was conducted 72 hours post-CIRI,accompanied by Triphenyltet-razolium chloride(TTC)staining.Post-scoring,brain tissue specimens were collected for hematoxylin-eosin(HE)staining to observe neuronal pathological damage.Transmission electron microscopy was utilized to examine neuronal ultrastructure and autophagy.Immu-nofluorescence was employed for the detection of autophagic markers,and real-time fluorescence quantification,along with protein im-munoblotting,were performed to assess proteins and genes related to autophagy and calcium overload.The results indicate that 6-shog-aol can upregulate miRNA-26a-5p expression,inhibit DAPK1 expression,and alleviate excessive autophagy and calcium overload after CIRI in rats,showcasing its neuroprotective properties.
维普
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