目的 探讨黄芩苷通过抑制 PGE2 对脑缺血再灌注损伤（CIRI）小鼠神经炎症及认知功能 障碍的影响。方法 成年雄性 C57BL/6J 小鼠随机分组，行短暂双侧颈总动脉闭塞（tBCCAO）造模，给予 黄芩苷灌胃或侧脑室注射 PGE2 干预。水迷宫检测小鼠认知功能；ELISA 测定术后 72 h 海马脂质过 氧 化及神经炎症水平；HE 染色观察脑组织病理改变；Western blot 检测海马铁死亡相关蛋白 GPX4、 DMT1、PTGS2 表达。结果 CIRI 引起小鼠认知功能损害，并伴随海马神经元损伤、神经炎症、脂质过氧 化及铁死亡相关蛋白异常表达（P < 0.05）；黄芩苷预处理可改善 CIRI 引起的认知功能损害，并伴随海 马神经元损伤减轻，神经炎症、脂质过氧化、铁死亡相关蛋白异常表达减少（P < 0.05）。侧脑室注射 PGE2 后小鼠海马 PGE2 上调，并伴随海马神经炎症、脂质过氧化、铁死亡相关蛋白异常表达（P < 0.05）； 黄芩苷通过抑制 PGE2 上调减少海马神经炎症、脂质过氧化、铁死亡相关蛋白异常表达（P < 0.05）。 海马 PGE2 上调加重 CIRI 引起的小鼠认知障碍（P < 0.05）；黄芩苷通过抑制 PGE2 的上调改善认知功 能损害（P < 0.05）。结论 黄芩苷改善 CIRI 引起的认知功能损害，其机制与 PGE2 相关的神经炎症被 抑制有关。 

Objective To investigate the effects of baicalin on neuroinflammation and cognitive dysfunction in mice with cerebral ischemia-reperfusion injury （CIRI） by inhibiting PGE2. Methods Adult male C57BL/ 6J mice were randomly divided into two groups， the model of bilateral carotid artery occlusion （tBCCAO） was established. Baicalin was given by gavage or PGE2 was injected into lateral ventricle.The cognitive function of mice was detected by Morris water maze. The lipid peroxidation and neuroinflammation in hippocampus were measured by ELISA at 72 h after operation. The pathological changes of brain tissue were observed by HE staining. Western blot was used to detect the expression of GPX4， DMT1 and PTGS2 in hippocampus. Results CIRI induced cognitive impairment in mice， accompanied by hippocampal neuronal injury， neuroinflammation， lipid peroxidation and abnormal expression of ferroptosis associated proteins （P < 0.05）. Baicalin pretreatment could improve the cognitive impairment induced by CIRI in mice， and was accompanied by a reduction in hippocampal neuronal injury， neuroinflammation， lipid peroxidation and abnormal expression of ferroptosis associated proteins （P < 0.05）.PGE2 was upregulated in the hippocampus of mice after intracerebroventricular injection of PGE2， accompanied by neuroinflammation， lipid peroxidation and abnormal expression of ferroptosis associated proteins （P < 0.05）. Baicalin could decrease the neuroinflammation， lipid peroxidation and abnormal expression of ferroptosis associated proteins in hippocampus by inhibiting PGE2 up-regulation （P < 0.05）. The up-regulation of PGE2 in hippocampus aggravated the cognitive impairment induced by CIRI （P < 0.05）. Baicalin improved cognitive impairment by inhibiting the up-regulation of PGE2（P < 0.05）. Conclusion Baicalin ameliorates the cognitive impairment induced by CIRI， and the mechanism is related to the inhibition of PGE2-related neuroinflammation.