To investigate the mechanism of Angelica sinensis polysac-charide (ASP) ameliorating endometriosis (EMT) via the Kelch-like epichlorohydrin-associated protein 1 (Keap1)/nuclear factor-erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) pathway. SD rats were randomly divided into six groups (n=12 per group): normal control, model control, low-dose ASP, high-dose ASP, gestrinone, and high-dose ASP+recombinant Keap1 (rKeap1). EMT models were established in all groups except the normal control group. After successful modeling, the drugs were administered once daily for 4 weeks. The mass and volume of ectopic endometrial tissue were measured. Histopathological changes were evaluated using hematoxylin and eosin staining. Levels of reactive oxygen species, malondialdehyde, and superoxide dismutase (SOD) were measured using commercial kits. The number of autophagosomes was examined under transmission electron microscopy. The relative fluorescence intensity of microtubule-associated protein light chain 3 (LC3) in endometrial tissue was assessed by immunofluorescence staining. Western blotting was used to determine the protein expression levels of LC3-Ⅱ, LC3-Ⅰ, p62, Keap1, Nrf2 in the nucleus, and HO-1. Compared with the normal control group, the model control group showed increased glandular proliferation, pronounced vacuolization of glandular cells, and substantial inflammatory cell infiltration in ectopic endometrial tissue. Levels of reactive oxygen species, malondialdehyde, p62, and Keap1 were significantly increased, while SOD levels, autophagosome numbers, and LC3 fluorescence intensity were significantly decreased (all P<0.05). Protein expression levels of LC3-Ⅱ/LC3-Ⅰ, Nrf2 in the nucleus, and HO-1 were also significantly reduced (all P<0.05). Compared with the model control group, the low- and high-dose ASP groups and the gestrinone group exhibited alleviated pathological damages, reduced mass and volume of ectopic endometrial tissues, decreased levels of reactive oxygen species, malondialdehyde, p62, and Keap1, and increased SOD levels, autophagosome numbers, LC3 fluorescence intensity, and protein expression levels of LC3-Ⅱ/LC3-Ⅰ, Nrf2 in the nucleus, and HO-1 (all P<0.05). However, co-administration of rKeap1 reversed the inhibitory effects of high-dose ASP on oxidative stress and its restorative effects on autophagic homeostasis in EMT rats. Angelica sinensis polysaccharide may ameliorate EMT in rats by inhibiting Keap1-mediated activation of the Nrf2/HO-1 pathway, thereby suppressing oxidative stress and restoring autophagic homeostasis. 目的: 基于Kelch样环氧氯丙烷相关蛋白1（Keap1）/核转录因子红系2相关因子2（Nrf2）/血红素加氧酶1（HO-1）信号通路探讨当归多糖改善子宫内膜异位症（EMT）的机制。方法: SD大鼠随机分为正常对照组、模型对照组、小剂量当归多糖组、大剂量当归多糖组、孕三烯酮组、大剂量当归多糖+重组Keap1（rKeap1）组，每组12只。除正常对照组外，其他组均构建EMT模型，建模成功后，给药1次/d，持续4周。测量大鼠异位子宫内膜组织的质量和体积，苏木精-伊红染色观察子宫内膜组织病理学特征，通过试剂盒检测活性氧、丙二醛、超氧化物歧化酶（SOD）水平;透射电镜观察子宫内膜组织中自噬小体数;免疫荧光染色检测子宫内膜组织中微管相关蛋白轻链3（LC3）相对荧光强度;蛋白质印迹法检测子宫内膜组织中LC3-Ⅱ与LC3-Ⅰ比值及p62、Keap1、细胞核Nrf2、HO-1蛋白水平。结果: 与正常对照组比较，模型对照组异位子宫内膜组织腺体增多，细胞空泡化明显，炎性细胞浸润明显，活性氧、丙二醛水平及p62、Keap1表达增加，而SOD水平降低，自噬小体数减少，LC3相对荧光强度降低，LC3-Ⅱ与LC3-Ⅰ比值减小，细胞核Nrf2、HO-1表达减少（均P<0.05）。与模型对照组比较，小、大剂量当归多糖组及孕三烯酮组异位子宫内膜组织病理损伤减轻，异位子宫内膜组织质量和体积、活性氧、丙二醛水平及p62、Keap1表达减少，SOD水平升高，自噬小体数、LC3相对荧光强度增加，LC3-Ⅱ与LC3-Ⅰ比值增大，细胞核Nrf2、HO-1表达增加（均P<0.05）。rKeap1逆转了大剂量当归多糖对EMT大鼠氧化应激的抑制作用以及对自噬稳态的恢复作用。结论: 当归多糖可能通过阻断Keap1激活Nrf2/HO-1信号通路，抑制大鼠氧化应激，恢复自噬稳态，从而改善EMT。.
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