为探究6-姜烯酚（6-Shogaol, 6-SH）对大鼠脑缺血再灌注损伤（cerebral ischemia-reperfusion injury, CIRI）的保护作用，采用分子对接观察6-SH能否自发性结合microRNA-26a-5p（miRNA-26a-5P），双萤光素报告基因检测验证miRNA-26a-5p与死亡相关蛋白激酶1（ceath associated protein kinase 1, DAPK 1）的靶向关系；线栓法制备大鼠CIRI模型，雄性SD大鼠随机为假手术组、模型组、6-姜烯酚组；于CIRI后72 h进行改良神经功能评分，氯化三苯基四氮唑（triphenyltetrazolium chloride, TTC）染色，评分后采集脑组织标本进行苏木精-伊红（hematoxylin-eosin staining, HE）染色观察神经细胞病理损伤情况，透射电镜观察神经元超微结构及自噬情况，免疫荧光检测自噬标志物，实时荧光定量和蛋白印迹法检测自噬和钙超载相关蛋白和基因。实验结果表明6姜烯酚可上调miRNA-26a-5p的表达，抑制DAPK1的表达，减轻大鼠CIRI后过度自噬和钙超载，发挥神经保护作用。

To explore the protective effects of 6-shogaol (6-SH) against cerebral is chemia-reperfusion injury (CIRI) in rats, molecular docking was utilized to investigate the spontaneous binding ability of 6-SH with microRNA-26a-5p (miRNA-26a-5P). Dual luciferase 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 Triphenyltetrazolium 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. Immunofluorescence was employed for the detection of autophagic markers, and real-time fluorescence quantification, along with protein immunoblotting, were performed to assess proteins and genes related to autophagy and calcium overload. The results indicate that 6-shogaol can upregulate miRNA-26a-5p expression, inhibit DAPK1 expression, and alleviate excessive autophagy and calcium overload after CIRI in rats, showcasing its neuroprotective properties.