目的 探讨瑞马唑仑（REM）对脑缺血再灌注损伤（CIRI）大鼠及腺苷酸活化蛋白激酶/核苷酸结合寡聚化结构域样受体蛋白3（AMPK/NLRP3）信号通路的影响。方法  取100只大鼠，构建CIRI大鼠模型并将其随机分为模型（Mod）组、瑞马唑仑低、中、高剂量组（REM-L、REM-M、REM-H）、瑞马唑仑高剂量+通路抑制剂（Compound C）（REM-H+Compound C）组，每组20只，另取20只健康大鼠作为对照（Ctrl）组。对所有大鼠进行神经行为学评分，分别检测脑含水量、脑梗死面积及脑组织氧化应激指标，HE和TUNEL染色分别观察脑组织形态和细胞凋亡，Western blotting检测AMPK/NLRP3信号通路有关蛋白表达。结果  与Mod组相比，随着REM剂量的增加，大鼠运动障碍减轻，脑组织整体结构逐渐恢复，病理损伤减轻，脑梗死面积减少、脑含水量以及细胞凋亡率降低，活性氧（ROS）水平、丙二酫（MDA）含量以及NLRP3和Caspase-1蛋白表达降低，超氧化物歧化酶（SOD）含量和AMPK蛋白表达升高（P＜0.05）；与REM-H组相比，REM-H＋Compound C组大鼠运动障碍加重，脑组织病理损伤较重，脑梗死面积、脑含水量和细胞凋亡率增加，ROS水平、MDA含量和NLRP3、Caspase-1蛋白表达升高，SOD含量和AMPK蛋白表达降低（P＜0.05）。结论  瑞马唑仑能够增强机体的抗氧化功效，减少脑细胞凋亡和减轻脑组织病损，对大鼠缺血再灌注脑损伤起治疗作用，其机制可能与激活AMPK/NLRP3信号通路有关。

Objective To investigate the effects of remimazolam (REM) on cerebral ischemia-reperfusion injury (CIRI) rats and the AMP-activated protein kinase (AMPK)/NOD-like receptor protein 3 (NLRP3) signaling pathway. Methods  One hundred rats were selected to construct the CIRI rat model(Mod) and stochastically separated into a Mod group, low, medium, and high dose remifentanil groups (REM-L, REM-M, REM-H), and high dose remifentanil+pathway inhibitor Compound C group (REM-H+Compound C), with 20 rats in each group. Another 20 healthy rats were included as the control(Ctrl) group. All rats were subjected to neurobehavioral scoring. The water content, infarct area, and oxidative stress indicators of brain tissue were detected. The morphology and apoptosis of brain tissue were observed by HE and TUNEL staining. Western blotting was applied to detect protein expression related to the AMPK/NLRP3 signaling pathway. Results  Compared with the Mod group, with the increase of REM dose, the movement disorders in rats were alleviated, the overall structure of brain tissue gradually recovered, pathological damage was reduced, the area of cerebral infarction, brain water content, and apoptosis rate of brain tissue cells decreased, reactive oxygen species(ROS) level, malondialdehyde(MDA) content, and NLRP3 and Caspase-1 protein expression levels decreased, superoxide dismutase the(SOD) content and AMPK protein expression level increased (P<0.05). Compared with the REM-H group, the REM-H+Compound C group showed aggravated motor disorders, and more severe pathological damage to brain tissue, the area of cerebral infarction, cerebral water content and apoptosis rate of brain tissue cells increased, the ROS level, MDA content and the protein expression of NLRP3 and Caspase-1 increased, while the content of SOD and the protein expression decreased (P<0.05).   Conclusion  Remimazolam can enhance the antioxidant function of the body, reduce brain cell apoptosis, alleviate brain tissue injury, and thus have a certain protective effect on ischemia-reperfusion brain injury in rats, the mechanism of which may be related to the activation of the AMPK/NLRP3 signaling pathway.