目的 探讨龙血竭总黄酮（SDF）调控活性氧（ROS）/硫氧还蛋白结合蛋白（TXNIP）通路介导的细胞焦亡改善大鼠脑缺血再灌注损伤（CIRI）的机制。     方法 实验大鼠随机分为对照组（Ctrl）、CIRI组、低剂量SDF组(SDF-L)、高剂量SDF组(SDF-H)和高剂量SDF+氧化三甲胺 (TMAO) 组（SDF-H+ TMAO），除对照组外，其余大鼠均需通过改良线栓法构建CIRI模型；对各组大鼠进行Zea Longa评分；ELISA检测血清炎症因子白细胞介素（IL）-1β、IL-18及氧化应激相关因子超氧化物歧化酶（SOD）、丙二醛（MDA）、谷胱甘肽过氧化物酶（GSH-Px）水平；流式细胞仪检测ROS水平；脑水肿测定；2,3,5-氯化三苯基四氮唑（TTC）染色检测脑梗死情况；HE染色检测脑组织病理变化；免疫组织化学染色检测焦亡效应蛋白消皮素D（GSDMD）的表达；Western blotting检测ROS/TXNIP通路相关蛋白表达。    结果 CIRI组较对照组脑组织可见更大范围的脑梗死，伴有轻微出血，且炎性细胞浸润明显，神经元变性坏死，排列稀疏紊乱，细胞核固缩及核仁裂解现象明显；Zea Longa评分、脑梗死体积、脑组织含水量、IL-1β、IL-18、ROS、MDA水平及GSDMD、TXNIP、核苷酸结合寡聚结构域样受体蛋白3（NLRP3）、凋亡相关斑点样蛋白（ASC）、Caspase-1表达升高，SOD、GSH-Px活性降低（P<0.05）；SDF-L组、SDF-H组较CIRI组脑组织病理损伤明显改善，Zea Longa评分、脑梗死体积、脑组织含水量、IL-1β、IL-18、ROS、MDA水平及GSDMD、TXNIP、NLRP3、ASC、Caspase-1表达降低，SOD、GSH-Px活性升高（P<0.05）；TMAO处理可部分逆转SDF对大鼠CIRI的改善作用。    结论 SDF可改善大鼠CIRI，与抑制ROS/TXNIP信号通路介导的细胞焦亡有关。 

Objective To explore the mechanism by which the sanguis draconis flavones(SDF) regulates the reactive oxygen species (ROS)/thioredoxin-interacting protein (TXNIP) pathway to mediate cell pyroptosis and improve cerebral ischemia-reperfusion injury (CIRI) in rats.    Methods The experimental rats were randomly divided into the control group(Ctrl), the CIRI group, the low-dose SDF group (SDF-L), the high-dose SDF group (SDF-H), and the SDF-H+ROS/TXNIP pathway activator, trimethylamine oxide（TMAO) group（SDF-H+TMAO）. Among them, except for the control group, the remaining rats all needed to establish the CIRI rat model by the modified suture method. Zea Longa scoring was performed on rats from each group. ELISA was used to detect the levels of serum inflammatory factors interleukin (IL)-1β, IL-18 and oxidative stress-related factors superoxide dismutase (SOD), malondialdehyde (MDA), glutathione peroxidase (GSH-Px). Flow cytometry was used to measure the ROS levels. Cerebral edema was detected. Cerebral infarction was detected by 2,3,5-triphenyl tetrazolium chloride （TTC）staining. HE staining was used to detect the pathological changes of brain tissue. Immunohistochemistry was used to detect the expression of pyrolytic effector protein dermolin D (GSDMD). Western blotting was used to detect the expression of proteins related to the ROS/TXNIP pathway.    Results Compared with the control group, a large area of cerebral infarctions were observed in the brain tissue of the CIRI group, accompanied by mild hemorrhage and obvious infiltration of inflammatory cells. Neuronal cells underwent degeneration and necrosis, with sparse and disordered arrangement. The phenomena of nuclear condensation and nucleolus lysis were obvious. The Zea Longa score, cerebral infarction volume, brain tissue water content, levels of IL-1β, IL-18, ROS, MDA, and the expressions of GSDMD, TXNIP, nucleotide-binding oligomerization domain-like receptor protein 3（NLRP3）, apoptosis-related punctate protein （ASC）, and Caspase-1 increased, while the activities of SOD and GSH-Px decreased (P<0.05). Compared with the CIRI group, the pathological damage of brain tissues in the SDF-L group and the SDF-H group was significantly improved. The Zea Longa score, cerebral infarction volume, brain tissue water content, levels of IL-1β, IL-18, ROS, MDA, and the expressions of GSDMD, TXNIP, NLRP3, ASC, and Caspase-1 decreased. The activities of SOD and GSH-Px increased (P<0.05); TMAO treatment partially reversed the improvement effect of SDF on CIRI in rats.    Conclusion SDF ameliorates cerebral CIRI in rats by inhibiting ROS/TXNIP pathway-mediated pyroptosis.