目的·探讨大黄素在阿尔茨海默病（Alzheimer's disease，AD）中的作用及其潜在机制。方法·将野生型C57BL/6J小鼠和3×Tg-AD小鼠分为6组：对照组（C57BL/6J小鼠）、AD组（3×Tg-AD小鼠）、大黄素25 mg/kg组（3×Tg-AD小鼠+大黄素25 mg/kg）、大黄素50 mg/kg组（3×Tg-AD小鼠+大黄素50 mg/kg）、大黄素100 mg/kg组（3×Tg-AD小鼠+大黄素100 mg/kg）和多奈哌齐组（3×Tg-AD小鼠+多奈哌齐3 mg/kg）。采用Morris水迷宫实验分析小鼠学习记忆能力，采用免疫组织化学法检测胶质纤维酸性蛋白（glial fibrillary acidic protein，GFAP）、葡萄糖调节蛋白78（glucose-regulated protein 78kDa，GRP78）和肌醇需求酶1α（inositol-requiring enzyme 1α，IRE1α）的表达，采用酶联免疫吸附试验（enzyme-linked immunosorbent assay，ELISA）分析脑组织中肿瘤坏死因子-α（tumor necrosis factor-α，TNF-α）、白介素-1β（interleukin-1β，IL-1β）和IL-6的含量，采用Western blotting检测NF-κB p65、p-NF-κB p65、p38、p-p38的蛋白表达。结果·与对照组相比，AD组小鼠认知能力下降，GFAP表达升高，TNF-α、IL-1β、IL-6含量增多，GRP78和IRE1α表达升高，NF-κB p65、p38磷酸化表达升高。与AD组相比，大黄素改善AD小鼠的认知能力障碍，抑制星形胶质细胞过度激活和神经炎症，并降低脑组织GRP78、IRE1α、磷酸化NF-κB p65和磷酸化p38的表达。结论·大黄素能有效改善AD小鼠认知能力障碍，其机制可能与抑制星形胶质细胞内质网应激介导的神经炎症有关。

Objective ·To explore the effects and potential mechanisms of emodin on Alzheimer's disease (AD). Methods ·Wild-type C57BL/6J mice and 3×Tg-AD mice were divided into 6 groups: Control group (C57BL/6J mice), AD group (3×Tg-AD mice), Emodin 25 mg/kg group (3×Tg-AD mice + Emodin 25 mg/kg), Emodin 50 mg/kg group (3×Tg-AD mice + Emodin 50 mg/kg), Emodin 100 mg/kg group (3×Tg-AD mice + Emodin 100 mg/kg) and Donepezil group (3×Tg-AD mice + Donepezil 3 mg/kg). The Morris water maze test was used to evaluate the learning and memory abilities of mice. The expression of glial fibrillary acidic protein (GFAP), glucose-regulated protein 78kDa (GRP78), and inositol-requiring enzyme 1α (IRE1α) was detected by immunohistochemistry. The levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and IL-6 in brain tissue were measured by enzyme-linked immunosorbent assay (ELISA). Western blotting was used to detect the expression of NF-κB p65, p-NF-κB p65, p38, and p-p38 proteins. Results ·Compared with the control group, mice in the AD group showed impaired cognition, increased GFAP expression, elevated levels of TNF-α, IL-1β and IL-6, and increased expression of GRP78 and IRE1α, along with enhanced phosphorylation of NF-κB p65 and p38. Compared with the AD group, emodin improved cognitive impairment of AD mice, inhibited astrocyte overactivation and neuroinflammation, and decreased the expression of GRP78, IRE1α, phosphorylated NF-κB p65, and phosphorylated p38 in brain tissue. Conclusion ·Emodin can effectively improve cognitive impairment in AD mice, which may be related to the inhibition of endoplasmic reticulum stress-mediated neuroinflammation in astrocytes.