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目的:探究七氟醚后处理对脑缺血/再灌注（ischemia/reperfusion, I/R）损伤大鼠的脑保护作用及对活性氧（reactive oxygen species, ROS）/硫氧还蛋白结合蛋白（thioredoxin interacting protein, TXNIP）/NOD样受体相关蛋白3（NOD-like receptor associated protein 3, NLRP3）信号通路的影响。方法:60只SD雄性大鼠按随机数字表法分为假手术组（sham组）、I/R组、七氟醚后处理组（SP组），每组20只。采用大脑中动脉线栓法制备脑I/R模型，SP组造模后即刻吸入2.4%七氟醚30 min。对各组大鼠进行神经功能缺损评分；获取大鼠脑组织，H-E染色和2，3，5-氯化三苯基四氮唑（2, 3, 5-triphenyltetrazolium chloride, TTC）染色观察组织病理学变化和脑梗死体积；分析大鼠脑水肿程度及血脑屏障通透性；TUNEL法检测脑组织细胞凋亡率；检测血清炎性因子（IL-1β和IL-18）及脑组织氧化应激指标[ROS、丙二醛（malondialdehyde, MDA）、超氧化物歧化酶（superoxide dismutase, SOD）和谷胱甘肽过氧化物酶（glutathione peroxidase, GPx）]的水平；Western blot法检测TXNIP/NLRP3通路相关蛋白[TXNIP、NLRP3、凋亡相关点样蛋白（apotosis-associated speck-like protein containing a CARD, ASC）、半胱氨酸天冬氨酸酶-1（cysteine aspartase, caspase-1）]的表达。结果:与sham组比较，I/R组大鼠神经功能缺损评分、脑梗死体积明显升高（n P<0.05），脑组织水肿程度及血脑屏障通透性也明显增加，脑细胞凋亡率升高（n P<0.05），血清IL-1β和IL-18含量明显升高（n P<0.05），脑组织中ROS和MDA含量及TXNIP、NLRP3、ASC和caspase-1蛋白表达水平均明显升高（n P<0.05），而GPx和SOD活性降低（n P<0.05）；与I/R组比较，SP组神经功能缺损评分和脑梗死体积降低（n P<0.05），脑水肿程度及血脑屏障通透性下降，脑细胞的凋亡率降低（n P<0.05），血清IL-1β和IL-18含量明显降低（n P<0.05），脑组织中ROS和MDA含量及TXNIP、NLRP3、ASC和caspase-1蛋白水平明显降低（n P<0.05），而GPx和SOD活性升高（n P<0.05）。n 结论:七氟醚后处理能够有效减轻大鼠脑I/R损伤，可能与其对ROS/TXNIP/NLRP3信号通路的抑制有关。“,”Objective:To explore the protective effects of sevoflurane postconditioning on cerebral ischemia/reperfusion(I/R) injury in rats and its effect on the reactive oxygen species (ROS)/thioredoxin interacting protein (TXNIP)/NOD-like receptor-associated protein3 (NLRP3) signaling pathway.Methods:According to the random number table method, a total of 60 male SD rats were divided into three groups (n n=20): a sham operation (sham) group, an I/R group and a sevoflurane postconditioning (SP) group. A model of cerebral I/R was established through middle cerebral artery suture, and the SP group inhaled 2.4% sevoflurane over 30 min immediately after modeling. Their neurological deficit scores were evaluated. The brain tissues were obtained and the histopathological changes and cerebral infarction volume were observed by hematoxylin-eosin (H-E) staining and 2, 3, 5-triphenyltetrazolium chloride (TTC) staining. The degree of brain edema and blood-brain barrier permeability in rats were analyzed. The apoptosis rate of brain tissue cells were detected by terminal-deoxynucleoitidyl transferase mediated nick end labeling (TUNEL) method. The levels of serum inflammatory factors, such as interleukin (IL)-1β and IL-18, and oxidative stress indicators of brain tissues, such as ROS, malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GPx) were detected. The expression of TXNIP/NLRP3 pathway related proteins, such as TXNIP, NLRP3, apoptosis-associated speck-like protein containing a CARD (ASC), and cysteine aspartase (caspase-1) were detected by Western blot.n Results:Compared with the sham group, the I/R group presented remarkable increases in neurological deficit score and cerebral infarction volume (n P<0.05), the degree of brain edema and the permeability of blood-brain barrier, the apoptotic rate of brain cells (n P<0.05), the levels of serum IL-1β and IL-18, the contents of ROS and MDA in brain tissues, and the levels of TXNIP, NLRP3, ASC and caspase-1 protein, as well as decreases in the activities of GPx and SOD (n P<0.05). Compared with the I/R group, the SP group presented remarkable decreases in neurological deficit score and cerebral infarction volume (n P<0.05), the degree of brain edema and the permeability of blood-brain barrier, the apoptotic rate of brain cells (n P<0.05), the levels of serum IL-1β and IL-18, the contents of ROS and MDA in brain tissues, and the levels of TXNIP, NLRP3, ASC and caspase-1 protein, as well as increases in the activities of GPx and SOD (n P<0.05).n Conclusions:Sevoflurane postconditioning can effectively relieve cerebral I/R injury in rats, which may be related to the inhibition of the ROS/TXNIP/NLRP3 signaling pathway.